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188 Cards in this Set
- Front
- Back
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Pathogen
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microbe that causes disease
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antigen
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material from a pathogen that is recognized by the immune system but that does not necessarily elicit an immune response
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innate immunity
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rapid, non-specific immune response
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adaptive immunity
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slower, specific immune response
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leukocytes
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blood cells
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lymphocytes
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specialized blood cells that mediate adaptive immunity
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primary organs
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where the cells of the immune system develop and arise
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secondary organs
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interact with antigens here
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thymus
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primary lymphoid organ for T-cell development
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bone marrow
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primary lymphoid organ for B-cell development.
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cytokines
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small secreted peptides that are used for intracellular communication between cels of the immune system
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chemokines
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subset of cytokines that specialized in regulating cell motility
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inflammation
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complex series of events induced by tissue damage; characterized by redness, pain, swelling and heat
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ELISA
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measure small amounts of hormones, drugs, and microbes in body fluids
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Western blot
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detects disease associated proteins
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Defensins
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originally isolated from frog skinb ased on ability to kill bacteria; small polypeptides (<10kDa) secreted at mucosal surfaces with direct bacteriocidal properties
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non-covalent forces that hold antigens/antibodies together
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1. electrostatic forces
2. hydrogen bonds 3. van der waals forces 4. hydrophobic forces |
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protein homology
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identity or similarity between domains in two or more proteins
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epitope
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three-dimensional face of an antigen which makes contact with the antibody
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what are the three main ways that antibodies provide protection?
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1. neutralization
2. opsonization 3. complement activation |
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ADCC (antibody-dependent cellular toxicity)
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antibody binding antigens on the surface of target cells sends downstream signals to cause cell to die by apoptosis
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IgG
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1. predominant Ig in serum
2. 4 subclasses 3. important for opsonization, complement, and ADCC 4. crosses placenta to protect fetus |
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IgM
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1. pentameric
2. first Ig produced in response to infection 3. good at complement activation |
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IgA
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1. tetravalent (dimeric)
2. predominant Ig in secretions 3. transported across epithelial cells via poly-Ig receptor 4. 10g of IgA secreted/day 5. found in breast milk supplying passive immunity to baby |
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IgE
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1. present in very low amounts in serum
2. binds to Fc receptors present on mast cells/basophils 3. levels increase in parasitic infection 4. can transfer allergy between individuals |
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antibody
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protein that binds an antigen
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antigen
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substance that is recognized by the immune system
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immunogen
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a substance that elicits an immune response
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epitope
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portion of the antigen recognized by the antibody
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hapten
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small molecular that by itself cannot induce an immune response but can be an antigen
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what makes a good immunogen?
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1. foreignness
2. size - bigger is better 3. complexity 4. susceptilbility to phagocytosis 4. genotype of host 5. route of administration - subcutaneous better than IV 6. dose - not too high, not too low |
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how do adjuvants enhance the immunogenicity of antigens?
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1. triggering the innate immune system
2. slowing release of antigen 3. promoting phagocytosis of antigen |
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polyclonal antibodies
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antibody preparations from immunized animals. consists of a complex mixture of different antibodies produced by many B-cell clones
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monoclonal antibodies
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homogenous antibody preparations produced in the lab. Consist of a single type of antigen binding site produced by a single B-cell clone
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avidity
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influenced by both affinity and valence of the interaction
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When do antibody-antigen lattices form?
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form with polyclonal antibody and antigen with multiple distinct epitopes
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isotypic determinants
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secondary antibodies that recognize portions of the constant regions that a characteristic of a particular antibody isotype
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allotypic determinants
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some secondary antibodies recognize portions of the antibody that are variable between different individuals.
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idiotypic determinants
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some secondary antibodies recognized unique portions of the variable domain of the antibody
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what are two important features of a myeloma cell?
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1. unlimited growth
2. cellular machinery to produce antibodies 3. able to be selected against using HAT medium |
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ELISPOT
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can be used to determine the number of cells within a sample that are secreting a particular cytokine
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immunoprecipitation
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detects specific proteins from a complex mixture
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immunofluorescence microscopy
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immunofluorescence microscopy can provide spatial information abut cells or molecules that react with antibodies
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flow cytometry
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determine the number of cells within a sample that react with a particular antibody or antibodies
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what are the functions of complement?
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1. opsonization
2. provoke inflammation 3. poke holes in membrane leading to lysis of bacteria |
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what are the three different complement pathways?
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1. classical pathway
2. lectin pathway - mannose binding lectin or ficolin binds carbs on pathogen surface 3. alternative pathway |
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what does complement lead to?
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1. inflammation
2. opsonization 3. immune complex clearance 4. B-cell activation 5. cell lysis |
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Order of complement components:
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C1, C4, C2, C3, C5, C6, C7, C8, C9
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Smaller/larger complement fragments
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Ca = smaller fragment, Cb= larger fragment
Exception: C2a - large fragment, C2b - small fragment |
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what is the function of C5a?
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1. neutrophil chemotaxis/activation
2. stimulation of prostaglandin and leukotriene production 3. degranulation of mast cells and basophils 4. release of histamine 5. increase of vascular permeability 6. activates the endothelium |
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allele
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two or more alternative forms of a gene
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terminal deoxynucleotide transferase (TdT)
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adds nucleotides during VDJ recombination
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what can trigger T-cell independent responses of B-cells? (no T-cell help needed)
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1. simple, repetitive antigens
2. mostly IgM 3. modest affinity 4. B-cells activated by direct BCR crosslinking 5. B-cells activated by TLRs |
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what is signal 2 for B-cells?
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CD40L on T-cell binding to CD40 on the B-cell
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how is class-switch recombination different from VDJ?
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1. does not require RAG 1/2
2. Does require DNA break repair machinery 3. requires at least part of each switch sequence 4. occurs as part of the antigen-dependent phase in secondary lymphoid organs |
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affinity maturation
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the increase in the average affinity of an antisera that occurs during the course of an immune response or with successive immunizations
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Why do Ig genes of activated B-cells show such a high rate of mutation?
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Answer: uses error-prone repair to repair dsDNA breaks (mutation rate is 1 mutation per 1000 nucleotide per cell division)
Requires enzyme: activation-induced cytidine deaminase (AID) - AID initiates DNA repair and DNA breaks that lead to somatic hypermutation and class switch recombination |
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inbred mice
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generated by repeated brother-sister matings, homozygous at every loci
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syngenic mice
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genetically identical at all loci
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congenic mice
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genetically identical except for a small genomic region
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MHC Class I and II genes for mice and humans
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Class I: humans - A,B,C
mice - K,D,L Class II: humans - DP, DQ, DR mice - I-A, I-E |
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genetic polymorphism
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many alternative forms of the same gene or alleles are present in a population
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mutation
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an alteration in the sequence of a gene as compared to the sequence of the predominant allele in the population
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haplotype
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the set of genes within a complex locus which are inherited as a group because they are linked on a chromosome
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endogenous pathway
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antigens from the cytosol are presented on MHC I to CD8 T-cells
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exogenous pathway
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antigens internalized through endocytosis or phagocytosis are presented on MHC II to CD4 T-cells
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kinase
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enzyme that attaches phosphate groups to specific amino acids of proteins (tyr, ser, thr)
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Initial events in TCR signaling
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1. TCR + CD4 or CD8 binds peptide: MHC
2. Lck and Fyn phosphorylate ITAMS on CD3 complex 3. Zap-70 binds to phosphorylated ITAMs on CD3-zeta chains 4. Lck and Fyn phosphorylate and activate Zap-70 5. Zap-70 initiates downstream signaling events |
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how does the T-cell initially bind APC
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through low affinity LFA-1:ICAM-1 interactions
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which cells mediate positive selection for T-cells?
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cortical epithelial cells
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which cells mediate negative selection in the thymus?
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Medullary epithelial cells and dendritic cells
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Aire
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transcription factor whose job is to drive expression of genes in the thymus
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what are the three types of professional antigen presenting cells?
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1. B-cells
2. macrophages 3. dendritic cells |
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Why are dendritic cells such good APC's?
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1. express both MHC I and II
2. start in the right place (tissues) 3. end in the right place (LN) 3. immature DCs are highly efficient at taking up antigens in the tissues 4. after maturation, mature DCs present antigens to T-cells in LNs 5. express co-stimulatory molecules 7. express TLRs and other innate receptors |
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what are the three mechanisms of tolerance?
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1. central tolerance - negative selection in the thymus
2. Anergy - takes place in the periphery, peripheral tolerance 3. Tregs - regulatory T-cells (CD4+, CD25+) |
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FoxP3
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Transcription factor necessary for T-regulatory cell development
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Th1 cells
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produce IFN-gamma and IL-12
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Th2
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produces IL-4, IL-5, and IL-13
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Th17 cells
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produce IL-17, IL-21, and IL-22
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autocrine
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cytokine acts on producing cell
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paracrine
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cytokine acts on neighboring cell or cells
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endocrine
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cytokine acts on distant cells
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Th1 responses
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activates macrophages, induces B-cells to class switch to IgG2, and helps CTL differentiation; good at fighting intracellular bacteria/viruses
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Th2 responses
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induces B-cells to class switch to IgE, induces eosinophil differentiation and activation; good at fighting large parasites and worms
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Th17 responses
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important at mucosal surfaces, induces neutrophil recruitment, specific role in B-cell class switching is unclear; good at fighting extracellular bacteria and fungi
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perforin
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pore forming protein
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granzymes
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serine proteases involved in target cell death (granule enzyme)
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cathepsin B
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protease that cleaves perforin thereby preventing the perforin from poking holes in membrane of CTL
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what is inflammation characterized by?
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1. redness
2. pain 3. swelling 4. heat |
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what are the three way inflammation is initiated?
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1. complement
2. activation of macrophages 3. plasma enzyme activators |
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how do pathogens initiate inflmmation directly?
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1. PAMPs bind to PRRs on macrophages and dendritic cells
2. activation of TLRs and production of inflammatory cytokines |
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what are two types of anti-inflammatory drugs?
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1. steroids
2. NSAIDS |
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selectins
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bind to mucin-like CAMs; have lectin domain which binds to CHO.
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P-selectin
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found on endothelium
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E-selectin
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found on endothelium
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L-selectin
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found on neutrophils and lymphocytes
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Mucin-like CAMs
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bind to selectins; expressed on endothelium as signal for cells to exit bloodstream
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Ig-superfamily
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binds integrins; expressed on endothelium and APCs
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chemokines
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chemoattractant cytokine
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extravasation
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cells leaving the bloodstream
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function of IFN-alpha and IFN-beta
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1. induce resistance to viral replication in all cells
2. increase MHC I expression and antigen presentation in all cells 3. activate NK cells to kill virally infected cells |
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characteristics of immature DCs
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1. highly endocytic
2. weak stimulators of T-cells 3. low expressors of MHC and co-stimulatory molecules |
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characteristics of mature DCs
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1. not very endocytic
2. high expressors of MHC and co-stimulatory molecules 3. potent stimulators of T-cells |
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memory cell phenotype
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CD44+ (humans - CD45RO+)
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naive T-cell phenotype
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CD44-
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what are the two hypotheses for memory T-cell formation?
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1. separate set of T-cells from the start, pre-committed to becoming memory T-cells
2. responding T-cells are identical in potential, but after infection occurs, some mechanism selects a few cells to ultimately become memory cells instead of effector cells |
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M-cells
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take up antigen in the lumen by endocytosis/phagocytosis and transport the antigen to the basal membrane (transcytosis)
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what are the functions of IgA?
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1. secreted IgA on the gut surface can bind and neutralize pathogens/toxins
2. IgA is able to bind/neutralize antigens internalized in endosomes 3. IgA can export toxins and pathogens from the lamina propria while being secreted |
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what are the features of commensal bacteria?
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1. no TLRs expressed at the apical membrane of epithelial cells
2. lack virulence factors 3. lack ability to resist killing 4. can prevent local inflammatory response |
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Chron's disease
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inappropriate response against commensal bacteria
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X-linked agammaglobulinemia (XLA)
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no mature B-cells; people with this get recurrent infection with extracellular bacteria
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env
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HIV gene encoding envelope glycoprotein gp160 which is a precursor protein that splits into gp120 and gp41
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gag
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HIV gene encoding nucleocapsid proteins p24, p17
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pol
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HIV gene encoding RT, protease, and integrase
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what are some mechanisms that make certain individuals resistant to HIV?
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1. 32 bp deletion in CCR5 gene
2. Individuals with increased levels of chemokines that bind to CCR5 have reduced levels of viral replication and may have greater resistance to infection |
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Type I hypersensitivity
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IgE mediated, classic allergy
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Type II hypersensitivity
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IgG, IgM mediated - rbc lysis
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Type III hypersensitivity
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IgG mediated - immune complex disease
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Type IV hypersensitivity
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T-cell mediated, delayed-type hypersensitivity
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allergens
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non-parasite antigen that can stimulate a type I hypersensitive response
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Der P1
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enzyme allergen from fecal pellets of dust mites; breaks down components of tight junctions
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atopy
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genetic trait to have predisposition to localized anaphylaxis
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what are some potential risk factors for asthma?
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1. changes in exposure to infectious diseases
2. environmental pollution 3. allergen levels 4. dietary changes |
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autoimmunity definition
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immune response to self-antigens resulting in disease
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B-cell tolerance
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no T-cell help
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T-cell tolerance
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1. clonal deletion - negative selection in thymus, deletion in periphery
2. sequestration of antigens inside nucleus 3. immunological ignorance - self antigens at low density on APCs 4. anergy - lack of co-stimulation 5. suppression - Tregs |
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how does one induce autoimmunity?
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1. break of self tolerance by release of sequestered antigens
2. antigenic (molecular) mimicry 3. inappropriate expression of MHC II |
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autoimmune hemolytic anemia
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antibodies to rbc antigens
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goodpasture's syndrome
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autoantibodies to type IV collagen
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grave's disease
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autoantibodies to surface receptors (hyperthyroid)
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Hashimoto's thyrioditis
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hypothyroid; blocking autoantibodies inhibit thyroid function
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Mysathenia gravis
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autoantibodies to acetylcholine receptors block muscle activation and trigger inflammation that causes destruction of the nerve/muscle junctions resulting in paralysis
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rheumatoid arthritis
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autoantibodies to ubiquitous antigens
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systemic lupus erythematosus (SLE)
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chronic IgG production to intracellular proteins
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what are the susceptibility factors for autoimmunity?
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1. MHC type
2. gender 3. immune regulation genes 4. environmental factors |
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autograft
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graft on same animal
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isograft
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tissue transfer between genetically identical animals (ex. twins)
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allograft
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graft between genetically different members of the same species
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xenograft
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graft between different species
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hyperacute rejection
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pre-existing antibodies to graft
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acute rejection
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antibody/T-cell mediated
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chronic rejection
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CD4/CD8 T-cell mediated
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what are some tissue typing assays?
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1. microcytoxicity assay - donor and recipient cells tested with antibodies against MHC; complement is added and cell lysis is measured
2. flow cytometry - monoclonal antibodies to different MHC alleles to ID what MHC alleles are expressed by donor/host 3. mixed lymphocyte reaction - incubate host blood cells with irradiated donor blood cells |
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what are the three therapy targets to prevent rejection of grafts?
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1. block calcineurin
2. inhibit cell division 3. immune blockade |
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proto-oncogenes
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proteins that normally contribute positively to the initiation/execution of cell division
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tumor suppressor genes
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proteins that prevent the unwanted proliferation of mutant cells
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what are some mechanisms of tumor escape?
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1. antigen loss
2. loss of MHC or TAP 3. production of inhibitory cytokines such as TGF-beta 4. expression of FasL |
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what are two way to identify tumor antigens?
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1. biochemical ID - purify MHC from tumor cells, elute peptides, isolate peptides by HPLC and determine sequence
2. use T-cell clones to screen tumor cell cDNA library. |
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what are the four types of tumor antigens?
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1. re-expressed embryonic antigens
2. differentiation antigens - overexpressed normal proteins 3. viral antigens 4. mutated self-proteins - point mutations of normal cellular genes |
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what are the reasons for the rapid and vigorous response of memory T-cells?
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1. expanded numbers - up to 10^6/mouse spleen compared to naive animal
2. respond more rapidly than naive T-cells and within a few hours of restimulation they are cytotoxic and produce IFN-gamma 3. more sensitive to antigen - somewhat lower doses of antigen suffice to activate them compared to naive T-cells |
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how do memory B-cell responses differ from naive B-cell responses?
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1. increase in affinity
2. increase in number 3. increase in isotype switching |
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What are some possible mechanisms for CD4+ T-cell depletion in regards to AIDS?
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1. infected CD4+ T-cells killed directly by HIV or by virus specific CD8+ CTLs
2. cross-linking of CD4 by gp120 can cause T-cells to undergo apoptosis 3. gp120 may bind CD4+ T-cells in the thymus and interfere with positive selection |
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ways to diagnose HIV clinically?
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1. ELISA - measures antibodies to gp120
2. HIV viral RNA detected by PCR |
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how are CD4 T-cell counts measured?
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by flow cytometry
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viral load
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amount or viral particles measured in plasma PCR test detecting viral RNA
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what are the functions of complement?
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1. opsonization of cellular antigens
2. provoke inflammation 3. poke holes in membranes leading to lysis of bacteria 4. clear immune complexes 5. activate antigen-specific B-cells |
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classical complement pathway
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antigen:antibody complexes
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lectin pathway
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mannose binding lectin or ficolin binds carbohydrates on pathogen surface
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alternative pathway
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pathogen surfaces
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IgM
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secreted early upon infection, low affinity, broad specificity
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IgG
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secreted late upon infection, high affinity, highly specific
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ficolins
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specific pathogen carbohydrates
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mannose binding lectin
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particular spacing of mannose and fructose not found on mammalian cells
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what are the activities of activated C3?
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1. inflammation
2. opsonization 3. immune complex clearance 4. generation of the C5 convertase activity |
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what are the activities of C5a?
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1. neutrophils chemotaxis and activation (stimulation of prostaglandin and leukotriene)
2. degranulation of mast cells/basophils 3. increase of vascular permeability 4. activates the endothelium. |
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why is there immediate rejection when a pig heart is transplanted into a human?
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because of complement activation
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CD19
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B-cell specific transmembrane protein, Ig superfamily member. Large cytoplasmic domain binds to signaling molecules, associates in membrane with CR2 and alters signaling properties of BCR
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how is HIV activated?
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Transcription factors such as NF-kB can act on HIV enhancer regions to initiate transcription of viral DNA into RNA
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how is HIV transmitted?
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1. contact with rectal or genital mucosa with infected semen or vaginal secretions
2. injections of HIV infected blood 3. during pregnancy, childbirth or nursing |
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why are CTLs crucial for anti-HIV cell mediated immunity?
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1. emergence of HIV specific CTL during primary infection correlates with acute viral load reduction
2. HIV specific CTLs have been found with activity against env, gag, nef, and pol 3. CTL escape mutants of HIV have been identified 4. CTL produce high levels of cytokines MIP-1 alpha and beta and RANTES |
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What is the steady state model of infection for HIV?
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CD4 T-cell decline is a gradual losing of long immune struggle involving a cycle of:
1. CD4 T-cell infection 2. CD4 T-cell death 3. CD4 T-cell replacement Constant turnover of CD4+ T-cell drives the pathogenic process and constant viral replication contributes to development of HIV genetic variation. Finally, the CD4+ T-cell regeneration is exhausted, CD4+ T-cell number declines and AIDS develops |
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what do antivirals for HIV target?
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1. nucleoside chain terminantors
2. reverse transcriptase inhibitors 3. protease inhibitors which inhibit protein processing of large polyproteins |
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what are some of the issues with HIV vaccines?
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1. animal model not reproducible
2. HIV protein sequence variation 3. what immune response will provide protection? 4. need to identify good immunogens and stimulate immunity on mucosal surfaces |
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anaphylaxis
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symptoms such as hay fever, asthma, eczema, bee stings, and food allergies
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what are some candidate genes for a genetic predisposition to type I hypersensitivity (classic allergy)
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1. IL-4 receptor
2. IL-4 cytokine (promoter region to increase expression) 3. FceRI - high affinity IgE receptor 4. MHC II - present peptides promoting Th2 responses 5. inflammation genes |
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sensitization
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repeated exposure to allergens initiates immune response that generates IgE isotype
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what are some of the immediate effects of histamine?
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1. constriction of smooth muscle
2. vasodilation with increased fluid into tissues causing increased swelling or fluid in mucosa 3. activates enzymes for tissue breakdown |
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what are the primary mediators of type I hypersensitivity?
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1. histamine
2. cytokines TNF alpha, IL-1, IL-6 3. chemoattractants for neutrophils/eosinophils 4. enzymes tryptase, chymase, cathepsin |
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what are the secondary mediators of type I hypersensitivity?
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1. leukotrienes
2. prostaglandins 3. Th2 cytokines - IL-4, IL-5, and IL-13, GM-CSF |
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what role do eosinophils play in the continuation of sensitization
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drive late or chronic response; provide CD40L and IL-4 for B-cell activation
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what are some treatments for type I hypersensitivity?
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1. drugs - NSAIDS, anti-histamines, steroids, theophylline or epinephrine (prolongs cAMP levels in mast cells inhibiting degranulation)
2. immunotherapy - allergy shots (desensitization) |
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what are some treatments for type I hypersensitivity?
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1. drugs - NSAIDS, anti-histamines, steroids, theophylline or epinephrine (prolongs cAMP levels in mast cells inhibiting degranulation)
2. immunotherapy - allergy shots (desensitization) |
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what are some ways that tumors evade the immune system?
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1. antigen loss
2. loss of MHC or TAP 3. production of inhibitory cytokines 4. expression of FasL |
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what is the anti-tumor immune response?
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CTLs and NK cells important for getting rid of tumors
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ways to identify tumor antigens?
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1. biochemical - purify MHC, elute peptides, isolate peptides by HPLC and determine sequence
2. use T-cell clones to screen tumor cell cDNA library. Confirm with synthetic peptide of predicted sequence |
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sources of antigens that stimulate anti-tumor immune responses
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1. mutated oncogens, suppressor genes
2. new antigens generated by translocation (bcr/abl) 3. antigens derived from oncogenic virus 4. over-expressed normal differentiation antigen 5. re-expressed oncofetal antigen |
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what are the four types of tumor antigens?
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1. re-expressed oncogetal antigens (embryonic)
2. differentiation antigens - over-expressed normal proteins 3. viral antigens - oncogenic antigens 4. mutated self-proteins |
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what are some new targets of cancer treatments?
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1. receptor antagonists
2. protein kinase inhibitors 3. enzyme inhibitors 4. anti-sense oligonucleotides 5. anti-angiogenic factors |
