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91 Cards in this Set
- Front
- Back
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metaplasia
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change in mature cel type
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Positive selection of CD4+/CD8+ T-cells for interaction with self MHC-I or MHC-II molecules occurs in the:
A. lymph nodes B. spleen C. thymus D. bone marrow E. all of the above |
c
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After internalizing a protein antigen, B cells process this antigen
A. complexed with MHC class II molecules and present it to CD8+ T cells. B. complexed with MHC class I molecules and present it to CD8+ T cells. C. complexed with MHC class II molecules and present it to CD4+ T cells. D. complexed with MHC class I molecules and present it to CD4+ T cells. E. B cells produce antibodies only and do not have MHC receptors |
c
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The primary usefulness of somatic hypermutation in B-cells is to:
A. delete self reactive clones B. generate immunologic diversity C. increase antibody affinity D. induce heavy chain class switching |
c
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A naïve lymphocyte is one that:
A. has never circulated through the lymphatic system B. is immunocompetent but has not encountered antigen C. is tolerant to antigen D. lacks antigen specificity |
b
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Langerhans cells of the skin are a specialized dendritic cell in epidermis. Their primary function is in:
A. antigen processing for adaptive immunity B. delivery of melanin to keratinocytes C. immediate local host defense against pathogens D. mediating type I hypersensitivity in skin |
a
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patient develops Staphylococcal cellulitis of the leg. Which of the following represents the most likely sequential anatomical path bacteria might follow if they entered a lymphatic vessel in the affected area? (nb: entry to superior vena cava implies consequent spread into the arterial system)
A. afferent lymphatic to regional lymph node to spleen to thoracic duct to superior vena cava B. afferent lymphatic to regional lymph node to thoracic duct to superior vena cava to spleen C. afferent lymphatic to spleen to thoracic duct to regional lymph node to superior vena cava D. afferent lymphatic to superior vena cava to thoracic duct to regional lymph node to spleen E. afferent lymphatic to thoracic duct to regional lymph node to superior vena cava to spleen |
b
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Which of the following reactions that might occur in the skin would be most closely associated with a Type I immune response?
A. atrophy B. fibrosis C. granuloma D. urticaria E. vasculitis |
Type I reactions cause increased vascular permeability, primarily as a consequence of histamine release by mast cells, but not vasculitis. Vasculitis is defined by inflammatory cell infiltration and injury to the blood vessel directly. These are totally different situations.
Points Earned: 0/1 Correct Answer: D Your Response: E |
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As shown in the above figure, the typical serologic (= antibody response measured in serum) course following Hepatitis E virus (HEV) infection has been characterized using experimental models of infection in nonhuman primates and human volunteer studies. (The red ALT labeled line represents enzyme indicative of liver injury.) Two class-specific (immunoglobulin heavy chain class) antibody responses to HEV (anti-HEV) following infection are shown by the yellow and blue lines. The titer of one declines rapidly during early convalescence; while the other persists indefinitely. Which line represents the IgM anti-HEV titer?
A. blue line B. yellow line |
b
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Based on information in the Journal Club paper for this week, which of the following interventions might be expected to increase resistance to TB infection in people of African, and possibly Asian, descent:
A. Taking oral vitamin D supplementation B. Receiving gene therapy to enhance cathelicidin mRNA expression C. Receiving 1,25(OH)2D3 supplementation. D. All of the above |
d
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The key feature of HIV infection that is relevant for its impact on adaptive immunity is the relative depletion of which cell type:
A. CD4 cells B. CD8 cells C. Dendritic cells D. Macrophages E. NK cells |
a
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The subcapsular sinus of a lymph node is filled with:
A. Blood B. Lymph C. Lymphocytes D. Macrophages |
b
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Which mechanism of immune tolerance occurs both centrally and peripherally?
A. Clonal deletion B. Clonal inactivation (anergy) C. Clonal suppression D. Receptor editing |
a
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An example of immune tolerance would be:
A. Apoptosis of a developing thymocyte because the cell fails to make a functional T cell receptor B. Lack of immune reaction against a self-antigen because the self-antigen resembles a microbial antigen C. Loss of adhesion molecules by neutrophils, so that the neutrophils cannot exit the blood into tissues D. Loss of responsiveness of a peripheral T cell that recognizes antigen in the absence of a second signal from an antigen-presenting cell |
d
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how to make a heavy chain of antibody?
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d-> j then DJ -> V - cut by Rag 1 or Rag 2 -> ligated by P or N nucleptodes
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how to make light chains
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only V+J
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what is the purpose of allelic exclusion?
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make a B cell that has only one heavy chain and one light chain
excludes lamda if kappa turned off (in light chain) only one allele of the IgG expressed in a single cel - other one turned off Purose: to make one kind of antibody -> once it sees antigen -> clonal expoansion allelic exclusion: a B cell transcribes only one type of heavy and one type of light hain |
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what makes up antigen binding site?
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both light and heavy chain -> combination gives you diversity
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B cell receptor goes thru hyper mutation to have higher binding to antigen after antigen bound
what is the process of this? |
in variable region -> 3 hypervariable parts (CDR)after meeting antigen the 2 that weren't very muated becoem more mutated at a higher rate
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IgM
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made first
low affinity activates the complement cascade |
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IgE
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allergic (activation of mast cells), parasites,
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IgA
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mucosal
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IgG
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cross placenta
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what happens after antigen binds to B cell receptor?
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B cell recieves signals to cause boht cell diviosn and prolferation -> tries to be more specifc via somatic hypermutation via singly nuceltoide substitutions in variab;e region -> leads to selection of B cells that make hih affinity antibodies -> high affinity antibodies -> less dependece on IgM -> class switching: produce antidoies with differet effector functions
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what does a T cell ned to recognize antigen?
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MHC and CD3 recognition
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steps
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somatic hypermuuation -> high binding -> class switichin
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What are the 3 APCS that present antigents to T cells?
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macrophages, B cells and dendritic cells
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How to make cytotoxic T cells?
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APCs prsent viral+self antigen on MHC II -> recognized by cytotoxic CD8 naeive cell -> IL-2 secreted by APC induces naieve CD8 to differentiate into mature cytotiic cell and proliferate -> goes and binds to other APCs presneting viral particles -> apopotosis
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what are the three kinda of signals that APCs deliver to naieve T cells?
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Ag on MHCII, CD28 on T cels binding to B7 on APC , and Il-2 secretion from APC to T cell
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stages of T cell develpoment
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made in bone marrow -> go to thymus -. in subcapsular region -> double ngetaice T cell (don't express either CD8 or CD4) -> cortex -. doulbe positive (expres both) -> but now go through positive selction where need to select partener (1 of the 12) -> once selection is completed the other CD is downregulated -> cell goes on to become CD8 -> then dendritic cells presents self protins -> and their reactive T cell partners apoptose (negative selection)
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superantigen
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bacteria secrete toxin that mimics foreign antigen -> binds to MHC clas II and and to T cell receptor -> outpouring of cytokines -. toxicity
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reposnse of a froeign vs self antigen
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woth self -. no acotvatio nof TLR and no activation of B7 on APC
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Th1 and CD8
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Th1 cell will help a dendritic cell become a better activator of naieve CD8 T cells by increasing expression of B7 and secrting Il-2
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the movement of fluid through tissues
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capillaries -> tisues -> Enters lymphatic vessel afferent lymphatic marginal sinus medullary sinus efferent lymphatic thoracic
duct rt. subclavian vein (vena cava) heart |
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what does a T cell ned to recognize antigen?
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MHC and CD3 recognition
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steps
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somatic hypermuuation -> high binding -> class switichin
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What are the 3 APCS that present antigents to T cells?
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macrophages, B cells and dendritic cells
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How to make cytotoxic T cells?
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APCs prsent viral+self antigen on MHC II -> recognized by cytotoxic CD8 naeive cell -> IL-2 secreted by APC induces naieve CD8 to differentiate into mature cytotiic cell and proliferate -> goes and binds to other APCs presneting viral particles -> apopotosis
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what are the three kinda of signals that APCs deliver to naieve T cells?
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Ag on MHCII, CD28 on T cels binding to B7 on APC , and Il-2 secretion from APC to T cell
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what does the blood bring?
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naieve APC -. tissues -> pickantigen -> lumpahicts -> lymph node -> B cells -> b cells diff
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what happens when pahogen gets in?
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if they breach epithelium -> macs and dendirtic cells -> secrete cytokines that indice inflamm response -> go into MALT(all lining where the epithelium meet the outside) - gut, lungs
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what conects innate and adaptive immunity?
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antigen delivery via MHCs - could be in lymph node
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what makes sure that the antigens are sampled?
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lymph nodes - where APCS trvel to
and splkenn |
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functions of spleen
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filters blood - way for APCs and T cells already there there to respond to foreign antigen
clear old red blood cells by macd extramedullary hematopesis |
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sites of antigen processing and presenting
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spleen
MALT lymph nodes |
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types of MHC I - genes
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HLA A, B and C - all coexpressed
eah perosn expreses 6 different MHC I genes = alpha and beta2 receptor |
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MHC class II genes
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HLA DP, DQ, DR
= recptor have alpha and beta |
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intearction of peptide to MHC complex
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low affinity but slow off rate ->once bound stay on for long time
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where cna you see MHC I
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on all cell with nucleus (xcept for RBCs) - but the level of expresion will difer
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where can you see MHC class II
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on cells of immune system - esp on APCs
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INF- gamma
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increases expression of MHC class I and II molecules
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MHC restrition
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during positive seltion T cell choses a speciifc MHC and antigent to partner up with
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process of make a vaccine for thymus indepent antigen (TI-2)
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trick immune system into making T-dependint antibodies: polysacchardie with potien -> binds to B cell with polysaccharide -> protien gets degarde and presented to T cell -> induces B cell to make anitobdy for the polysachhardie antigen
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where can you see MHC class II
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on cells of immune system - esp on APCs
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INF- gamma
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increases expression of MHC class I and II molecules
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MHC restrition
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during positive seltion T cell choses a speciifc MHC and antigent to partner up with
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process of make a vaccine for thymus indepent antigen (TI-2)
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trick immune system into making T-dependint antibodies: polysacchardie with potien -> binds to B cell with polysaccharide -> protien gets degarde and presented to T cell -> induces B cell to make anitobdy for the polysachhardie antigen
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what is the innate resposne to epstein bar virus?
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stimulates IFN-alpha and beta to prevent viral replication and increase MHC-I and activate NK cells
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what is the adaptive repossne to epstein barr virus?
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viral capsid antigen goes into B cells and produces: EBNA and latent membrane protein (LMP-
stimulates B cell proliferation) *APC presents EBNA on MHC-I: that activates CD 8 T cells |
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what does INF -alpha and gama ue?
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induce resustacne to viral replication in all cellc
increases MHC class I expression and antigen presentation in all cells acitvate NK cells to kill virus-infected cells |
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type 1 hypersensisitivity
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allergy and anaphylasixz
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what happens in immediate hypersensiity - the allergic rxn
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IgE trigesr mast cell degranualtion upon second exposure -> release histamin -> NO -> vasodilation
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IgE
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allerigc and parasitic
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eosinophil
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in allergic rxn
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Type 2: antibody mediated hypersensitivity
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IgG or IgM - antigen is not soluble -> IgG goes and bind to it -> induces complement where gets phagoctized or can block signlaing of cell that is oresenting antigen -> paralyses the cell
like alloimune (attack foriegn RBCs) or automiine hemolytc anemia |
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Type 3 immune resopnse
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IgG antigen are soluble -> antibody-antigen compelx deposit on clel walls -> activate complemtn and inflamm
Ex: serum sivknes, rheumotiod arthristic, lupus, glomerulus nephritinis |
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type 4 imune reposne
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cell mediated T and B cells
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T cell mediated type 4 immune reposnse
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Th1 -> delayed type hypersensitiy
ex: poision ivy, TB test |
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cell mediated imune reposnse
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type4 T and B cells
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T cell immune reposne
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macrphage activation and cytotoxicity --via CD4 T cels
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B cell
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called cell mediated cytotoxicity: CD8 reocginize antigens on Class I -> kills virus infected cells
hepatitis |
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transplant rejection- what type of imune reaction
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Type 2, 3 9th1 -> recognize foreign peptide -> cyokines rlased -> triggers B cell and macrophage stimulation - this is type 4 ) and 4
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how does autoimmunty occur?
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from breakdown of tolerance
central (occurs during developemnt) and peripheral breakdown (occurs after meeting an antigen) |
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how does the body make sure it keeps this tolerance and prevent autoimmunty?
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receptor editing - anitgen rceptor undergoes mutaion so that self antigens aren't recognized
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to prevent development of autoimmune disease - what are the 4 mechanisms of tolerance
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1. clonal deletion(central in thymus, peripheral)
2. clonal anergy (T cell need second signal and B cell anergy - not enough receptors to respond) 3. peripheral supression: (Treg and denritic and T cells supress immune system) 4. immunological ignorance (T cell threshold ofr anitgen recognition not acgieved due to to little antigen presnet) |
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failure of tolerance -> autoimmuntiy
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1. failure of cloncal dltion: didn't make enough of transcription factor that says your self- AIRE
2. failure of clonal anergy (genetic mutaion in co-stiumation - have toom uch costimulation when you shouldn't) 3. failure of peripheral suppression (oral tolerance hasn't worked in humans) 4. failure in immune ignrance |
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what is the most common mechanism of autoimmunity?
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failure of immune ignorance:
via - creation of new epitopes (haptens and cryptic) mlecular mimicry (infectious agent has antigen similar to self- overcome anergy- production of cross reactive antibodies or T cells ) polyclonal lymphocyte activation (can have a superantigen -> polyclonal activation of autoreactive T cell -> overcome anergy) exposure of a sequesterd antigen |
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what are some events that can tip the balance to favor autoimunty?
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familial predispostion - dut to HLA type (can have failure in all types of immune response)
trauma infection puberty? |
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what are the two types of immunodeficieny?
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primary: have a specific genetic defect (T and B cells)
secondary: first get a condition and then autoimmunity |
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what is the key feature of HIV?
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loss of CD4
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what controls HIV?
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CD8 - when you take i away -> sharp increase in viremia - work by B14 recogniion sequence
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set point
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higher -> more rapid onset of AIDS
more prone to transmit the diases |
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why do we fail in HIV?
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virus mutates at point where it is recognized by cytotic t lymp
viruses's Nef protein -> downregulates MHC class I moleucle -> helps avoid immune system just mutates alot you also have clonal exhaustion - loss of pop of CTL due to senescence |
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bone marrow stem cells lineages
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hematocpoetic and mesenchymal
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where do embryonic stem cells come form?
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inner cell mass from blastocyst
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why do we fail in HIV?
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virus mutates at point where it is recognized by cytotic t lymp
viruses's Nef protein -> downregulates MHC class I moleucle -> helps avoid immune system just mutates alot you also have clonal exhaustion - loss of pop of CTL due to senescence |
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bone marrow stem cells lineages
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hematocpoetic and mesenchymal
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where do embryonic stem cells come form?
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inner cell mass from blastocyst
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ex of primary immunodeficeny
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CGD
myleperoxidase deficincy - can't kill intracellular bacteria , LAD defect |
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T cell defect
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thymic displasai - digeorgen sndrom - no stroma so no T cell development
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B cell defect
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agammaglobulinemia - no mature B cells being release form bone marrow -> no germinal centers
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