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94 Cards in this Set

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  • Back
Which genes code for MHC class I? What is the basic structure of the MHC class I protein?
There are three genes: A, B, and C. Each gene codes for an α subunit and a β subunit; the peptide binding cleft is determined by the α subunit (which has three domains).
Which genes code for MHC class II? What is the basic structure of the MHC class II protein?
There are three genes: DP, DQ, and DR. There is an α subunit and a β subunit, each of which have two domains. The peptide binding cleft encompasses both the α and β chain.
What is the difference in the way that peptides bind in the MHC class I groove and the MHC class II groove?
MHC class I binds short peptides (8-10 aa) by their ends, while MHC class II binds longer peptides, and in various places along the peptide. MHC class II is more restrictive in its binding.
Which cells express neither MHC class I nor MHC class II?
Red blood cells
How do dendritic cells take up antigen?
-macropinocytosis (primary)
-viral infection
Describe MHC expression on dendritic cells.
Immature dendritic cells (in tissue) have low MHC expression, while mature dendritic cells (in lymphoid tissue) have high MHC expression.
Describe MHC expression on macrophages.
Macrophages generally have low expression, but this increases to moderately high expression when stimulated by bacteria or cytokines.
Describe MHC expression on B cells.
B cells constitutively express moderately high levels of MHC. Upon activation, MHC expression further increases.
Which type of APC constitutively expresses co-stimulator?
Dendritic cells
What types of antigens do dendritic cells typically present?
-viral antigens
What types of antigens do macrophages typically present?
-particulate antigens
-intracellular pathogens
-extracellular pathogens
What types of antigens do B cells typically present?
-soluble antigens
How are antigens delivered to MHC class I for presentation?
An intracellular antigen is processed in the proteasome, the peptide is transported into the ER, the peptide binds to MHC class I in the ER, then MHC class I presents the peptide on the cell surface.
How are antigens delivered to MHC class II for presentation?
An extracellular antigen is processed in a phagolysosome. A vesicle containing MHC class II fuses with the phagolysosome, where the peptide binds to MHC class II. Then MHC class II presents the peptide on the cell surface.
What does calnexin do?
It binds partly folded MHC class I α chains in the ER until β2-microglobulin binds to them.
What does TAP do?
It delivers a peptide (manufactured by the proteasome) to the MHC class I molecule and completes its folding.
What does CLIP do?
CLIP is a short peptide fragment derived from Invariant chain (Ii) which binds in the groove of MHC class II, to prevent overloading of MHC class II.
What does HLA-DM do?
In the acidified endosome, it binds to MHC class II, which releases CLIP and allows a peptide to bind.
What is the difference between the expression of MHC alleles and of TCR alleles?
MHC alleles do not undergo rearrangement and are codominant; both are expressed. TCR alleles undergo V-J arrangement or V-D-J arrangement and exhibit allelic exclusion; after one allele is rearranged, the other is excluded from use.
What area of the MHC gene expresses polymorphism?
binding cleft
How does inbreeding contribute to the potential spread of a pathogen through a population?
Inbreeding reduces the diversity of MHC alleles, so it is more likely that a pathogen will spread through an inbred population due to inability of any MHC to bind that pathogen.
What is a potential benefit of having only three genes which code for each MHC class?
Reduces the likelihood of inappropriate recognition/destruction of self.
How is CD1 different from classical MHCs?
-instead of being targeted to ER, is targeted to vesicles
-can also present glycolipids (esp. components of mycobacterial membranes)
Why are TCR specificities non-heritable?
They result from somatic rearrangement, not germ-line rearrangement.
Why are developing T cells especially sensitive to DNA damaging factors?
Developing T cells are undergoing DNA rearrangement, which is sensitive to damage because DNA has to be broken and rejoined precisely.
What happens to T cells with high affinity for self peptides during thymic development?
Undergo apoptosis
What are the consequences of HLA-DM (H-2M) deficiency?
CLIP is not removed, so peptides cannot bind in the MHC class II groove. During thymic development, T cells specific for self peptides are not deleted, and there is an autoimmune response.
How do APC and T-cell interactions begin? How is the interaction stabilized?
ICAM-1 on an APC binds transiently to LFA-1 (or VCAM-1 binds to VLA-1). Binding of TCRs to MHC-antigen complexes signals LFA-1 to change conformation and strengthen the interaction.
What happens if a co-stimulatory signal interacts with a T cell without MHC?
What happens if MHC interacts with a T cell without a co-stimulatory signal?
inactivation of the T cell (anergy)
In what stage of T cell development is co-stimulation the most important? In what stage is it least important?
Co-stimulation is most important for naive T cells, and becomes less important as the T cell matures.
What types of cells are usually involved in chronic inflammation?
-plasma cells
What are the three components of chronic inflammation?
What is subacute inflammation?
Periods of acute inflammation are alternated with healing; both acute and chronic inflammatory cells are present.
How are helminthic infections handled by the immune system?
B cells release IgE, which binds to the parasite. Then eosinophils use the Fc receptor to interact with the parasite and release Major Basic Protein, which will help kill it.
What are epithelioid cells?
Macrophages which are not able to phagocytose the foreign material, and are flat as a result; they resemble epithelial cells.
What are giant cells? What are the two different types and how can you tell them apart?
Giant cells are formed by the fusion of epithelioid cells, and have lots of nuclei (sometimes up to 50).
-Langhans giant cells: nuclei around periphery
-foreign body giant cells: nuclei centrally located or scattered
What are granulomas?
A collection of epithelioid cells (always), surrounded by lymphocytes (usually), giant cells (frequently), fibroblasts, plasma cells, and macrophages (possibly), and neutrophils (occasionally).
What is the difference between a granuloma and a tubercule?
A tubercule has necrosis in the center, a granuloma hasn't.
What are the two factors that generally contribute to granuloma formation?
-presence of indigestible organisms or particles
-immunity to the inciting agent
What is the difference between regeneration and repair?
Regeneration is the replacement of lost cells by the same cell type, while repair is the replacement of lost cells by connective tissue.
What is granulation tissue?
Tissue in a healing wound that has proliferation of fibroblasts and new blood vessels, with macrophages and mast cells always present.
What are the basic steps in angiogenesis?
-degradation of the basement membrane of the mother vessel to allow a new branch to form
-migration of the existing vascular endothelial cells into the new sprout
-proliferation, forming a solid cylindrical outgrowth coated by fibronectin
-formation of a new lumen + basement membrane within the new vessel
-vessels encounter each other, circulation forms
How does healing by first intention differ from healing by second intention?
-injury: primary union - little or no tissue defect, secondary union - large tissue defect
-inflammation: more for secondary union
-first intention has ordered sequence of events, second intention does not
-second intention generates more granulation tissue and it persists longer
-in second intention healing, surface wounds undergo wound contraction
Which factors retard wound healing?
-protein deficiency
-oxygen tension
-cooler temperatures
-infection, foreign material
-mobility of tissue
Which factors promote wound healing?
-growth factors
What is the difference between an antibody and a B cell receptor?
-Antibodies are secreted, so the C-terminus is hydrophilic.
-BCRs are membrane-bound, so the C-terminus is hydrophobic.
Otherwise, they are the same.
What is the purpose of the constant region of the antibody?
Interacts with effector cells and other mediators.
What are the forces that bind antigens and immunoglobulins?
-Van der Waals
-hydrophobic interactions
What do RAG protein complexes do?
Initiate somatic recombination by binding to and cleaving recombination signal sequences
At what point in B cell development are the heavy chain genes finished rearranging? What is on the cellular surface at this stage?
Large pre-B cell; μ chain is on the surface (transiently)
At what point in B cell development are the light chain genes finished rearranging? What is on the cellular surface at this stage?
Immature B cell; IgM is on the surface
How is an immature B cell distinguishable from a mature one?
Immature B cells only have IgM; mature B cells have IgM and IgD.
What happens to B cells which have a high affinity for self molecules in the bone marrow?
Which immunoglobulin types can form multiplers? What is the purpose of forming multiplers?
Forming multiplers partially offsets lower affinity.
Which immunoglobulin is most abundant in serum? Least abundant?
IgG1 is most abundant. IgE is least abundant.
Which immunoglobulins are involved in the classical complement pathway? In the alternative?
IgG and IgM are involved in the classical pathway. IgA is involved in the alternative pathway.
Which immunoglobulin can pass through the placenta?
Which immunoglobulins bind to the Fc receptors of phagocytes?
Which immunoglobulin is reactive with staphylococcal Protein A?
Which immunoglobulins come from the same RNA transcript? How are they differentially expressed?
They start with the same RNA molecule, but are spliced differently.
What determines whether a cellular developmental event is reversible?
-If development involves DNA recombination or mutation, it is irreversible.
-If development only involves RNA splicing, it is reversible.
What do thymus-dependent and thymus-independent activation of B cells have in common? How are they different?
Both require antigen to bind BCR as the first signal.
-Thymus-dependent requires signal from T helper cell.
-Thymus-independent requires signal from TLRs or crosslinking of surface IgM.
How do mature B cells get to the lymph node? How do they leave?
Mature B cells get to the lymph node through the bloodstream. They leave via the efferent lymphatic vessel.
Where in the lymph node do B cells get activated? What do they do after that?
B cells get activated on the T cell/B cell border. Then they form primary foci in the medullary cords, or migrate to the primary follicle and form a germinal center (divide).
Where in the spleen do B cells get activated? What do they do after that?
B cells get activated in the T cell zone. Then they migrate to the T cell/red pulp border, and form primary foci and plasmablasts.
How do antibodies become more specific to the antigen as the immune response progresses?
Somatic hypermutation of antibody variable region. B cells with less specific mutations undergo apoptosis, while those with more specific mutations are stimulated to divide.
How are plasmablasts and resting B cells similar? How are they different?
-have surface IgG
-are APCs
-resting cell does not secrete IgG, plasmablast does
How are plasmablasts and plasma cells similar? How are they different?
-secrete IgG
-plasma cell has low surface IgG, plasmablast has high
-plasma cell is not APC, plasmablast is
-plasmablast can proliferate/differentiate, plasma cell can't
Which immunoglobulin type is important for mucosal immunity in the GI tract, nose, and lung?
What stimulates the development of TH1 cells? What inhibits it?
Stimulatory: APC presents peptide that binds strongly to TCR
Inhibitory: IL-10/TGFβ (secreted by TH2)
What stimulates the development of TH2 cells? What inhibits it?
-interaction between TCR and B cell MHC class II
-APC presents peptide that binds weakly to TCR
-IFN-γ (secreted by TH1)
What are some features of allergens that promote IgE response?
-protein (esp. MHC class II binding)
-enzymatically active
-low dose
-low molecular weight
-highly soluble
What steps in the immune response are usually targeted in allergy treatment?
-TH2 activation
-B cell activation
-mast cell activation
-mediator action
-eosinophil-dependent inflammation
What is a type I hypersensitivity response?
IgE recognizes a soluble antigen, then triggers mast cells to release inflammatory agents (i.e. allergy, asthma).
What is a type II hypersensitivity response?
IgG recognizes an antigen associated with a host cell or the matrix, then triggers complement or opsonizes the cell. If the antigen is a receptor, IgG alters signaling.
What is a type III hypersensitivity response?
IgG forms an immune complex with a soluble antigen, which leads to inflammation, phagocytosis, and blood vessel occlusion.
What is a type IV hypersensitivity response?
T cells interact with soluble or cell-associated antigen, and either secrete cytokines (inflammation) or cytotoxic factors (necrosis).
What is the difference between primary and secondary immunodeficiency?
Primary is usually of genetic origin. Secondary is due to aging, infection, or immunosuppression.
What is the difference between Leukocyte Adhesion Deficiency I and II?
LAD I is an integrin deficiency, LAD II is a selectin deficiency.
What is X-linked SCID?
Mutation in the gene for the gamma chain of IL-2 receptor → T cells do not develop → B cells do not develop.
How do defiencies in ADA lead to SCID?
Purines accumulate in cells, they are especially toxic to immature lymphoid cells → T and B cells do not develop.
How do deficiencies in DNA repair enzymes lead to SCID?
Maturation of T and B cells involves DNA rearrangement (variable region of receptors). Without DNA repair enzymes, this is not possible.
What is DiGeorge Syndrome?
A deletion in chromosome 22 causes lack of development of 3rd and 4th pharyngeal pouches → defective or missing thymus gland.
What is the phenotype of patients with B cell defects?
Recurrent bacterial and parasitic infections.
What is X-linked agammaglobulinemia?
Defect in Burton's tyrosine kinase → mature B cells are not released from bone marrow → no germinal centers in lymphoid tissues and no serum Ig
What is hyper IgM syndrome?
X-linked T cell defect prevents B cell maturation, no germinal centers in lymphoid tissues, and only serum IgM is present.
How does TNF contribute to septic shock?
-macrophages throughout the body release TNF in response to pathogen
-TNF leads to vasodilation and decrease in plasma volume
-TNF causes systemic coagulation, using up clotting factors
What is the systemic effect of cytokines produced by macrophages (TNF, IL1b, IL6)? What is the local effect?
Systemic: induce fever
Local: induce acute-phase response (shift in proteins produced by liver)
What do IFN-α and IFN-β do? What induces their synthesis?
-interfere with viral replication
-increase MHC class I expression and antigen presentation in all cells
-activate NK cells
TLR3, which recognizes double stranded RNA, induces IFN synthesis
What does an intestinal epithelial cell do when it is infected?
Express MIC-A and MIC-B, which bind to NKG2D receptor on NK T cells. The NK T cells induce apoptosis of the infected cell.
How is foreign MHC from a trsnsplant recognized by the host immune system?
Two ways:
-foreign MHC interacts directly with host TCR
-host APC processes foreign MHC and presents to TCR
How do corticosteroids prevent transplant rejection?
-adhesion molecules
What does Ziehl Neelson (acid fast) stain do?
stains Mycobacterium tuberculosis