Flashcards in Immunology Deck (49):
What cytokines are secreted by TH1 cells?
What cytokines are secreted by TH2 cells?
IL-4, IL-5, IL-10, IL-13
What is a granuloma, what mediates its development?
Defined by the presence of a collection of epithelioid histiocytes. May also contain giant cells (multinucleated cells formed by the fusion of multiple epithelioid histiocytes; may also be surrounded by a ring of lymphocytes.
INF-g, secreted by TH1 cells, is the mediator of macrophage transformation into epithelioid histiocytes that occurs in granulomatous inflammation.
What test can be used to determine the presence of antibodies in a patient's serum?
What test detects the presence/levels of RNA in a cell?
What test is used to detect presence/level of DNA?
What immune cells exit the blood/leave circulation early in infection? What molecules mediate this process?
IL-8, C5a, LTB4, bacterial products (e.g.; f-met peptides)
What type of hypersensitivity does the tuberculin skin test demonstrate?
Type IV Hypersensitivity-- a cell-mediated immune response involving CD4+ TH1 cells activating and attracting macrophages to the area. The most important cytokine stimulating this response is INF-g that is secreted by the TH1 cells to activate the macrophages.
The TB skin test is a classic demonstration of the function of the cell-mediated arm of the immune response (as opposed to the humoral immune response).
What is the Arthus Reaction?
This is an example of Type III Hypersensitivity--disease caused by antigen-antibody immune complexes.
The Arthus reaction is induced by subcutaneous administration of a protein antigen to a previously immunized individual. It results in the formation of immune complexes at the site of antigen injection, and a local vasculitis.
the passage of blood cells through the intact walls of capillaries, typically accompanying inflammation
Which immune system cells are always the first responders to any injury?
After 48 hours, would neutrophils be the predominant cell at the site of infection/injury?
What is the predominant cell at the site of infection/injury after 48 hours?
What are LAK cells?
These are NK cells that have been activated by IL-2. They are considered to be super-activated NK cells.
What is the role of NK cells?
They function in killing altered self cells, such as tumor cells or virus-infected cells. They participate in ADCC (antibody-dependent cellular cytotoxicity)
On which cells is CD19 found?
On which cells is CD16 found? what is its function?
NK cells, macrophages, mast cells
It is an Fc receptor; functions in ADCC
Where is CD3 found? What is its purpose?
On T cells and thymocytes.
It is part of the TCR (g,d,e,z subunits) and is involved in signal transduction by the TCR
What would happen if a patient's cells lacked MHCII expression?
The patient would lack CD4+ t cells. During positive selection in the cortex of the thymus, only those cells that can recognize antigen presented on MHC proteins will be rescued from cell death. Without MHC class II proteins, no CD4+ cells will develop/be rescued. This patient will still be able to make CD8+ cells, but because Th cells are important in virtually all immune responses (humoral and cell-mediated, for example), the lack of CD4+ cells will affect the patient's ability to respond to intra- and extracellular pathogens.
What two receptors are found on NK cells? (differentiate NK cells)
CD 16 and CD56
What is another name for the complement proteins C5a and C3a?
Draw the mechanism of oxygen-dependent killing in phagocytes.
What is the result of an NADPH oxidase defect?
Chronic Granulomatous Disease. These patients cannot produce superoxide from oxygen, and therefore cannot produce the hydorgen peroxide necessary for the production of halide radicals (like bleach). These patients will be predisposed to infection with catalase positive bacteria, as these bacteria can destroy the hydrogen peroxide that they naturally produce, leaving none for the host cell with which to produce the halide radicals via myeloperoxidase
What does the Nitroblue Tetrazolium (NBT) test look for? How is it interpreted?
This test asks the question: Do we have the ability to convert oxygen to superoxide. i.e.; do we have functional NADPH oxidase?
The Nitroblue Tetrazolium turns blue. This means we have functional NADPH oxidase, and can convert oxygen to superoxide
The rxn remains colorless/yellow; NADPH is absent/defective
What is the most common cause of severe combined immunodeficiency disease (SCID)?
A defect of IL-2 receptors
What is a xenograft?
a transplant between members of different species (e.g., a human receiving a pig heart valve)
What is an allogeneic graft?
a transplant between two members of the same species who are not genetically identical
What is an autograft?
a graft from one location to another on the same individual
What is an isograft?
a graft of tissue between two individuals who are genetically identical. These individuals would have the same MHC proteins. Tissue rejection in this case is virtually unheard of.
What type of hypersensitivity response is chronic graft rejection?
Type IV hypersensitivity
In adults, what would significant numbers of cells co-expressing CD4 and CD8 imply?
Non-Hodgkin lymphoma, with a cell population similar to immature T cells.
What are the best cell surface molecules to identify B cells?
The best markers for the identification of B cells are:
CD19, CD20, and CD21
The CD21 molecule is a receptor for EBV (Epstein-Barr Virus)
What is the classic triad of symptoms in patients with Wiskott-Aldrich Syndrome?
Eczema, thrombocytopenia, and immunodeficiency.
More specifically, it presents as the clinical triad of thrombocytopenic purpura, eczema, and recurrent opportunistic infections with organisms that have polysaccharide capsules, such as Streptococcus pneumoniae.
What are the relative immunoglobulin levels in a patient with Wiskott-Aldrich Syndrome?
Patients characteristically have :
decreased serum IgM
What is hyper-IgM syndrome?
This is an X-linked immunodeficiency that is a mutation of the CD40L on activated Th cells that results in a deficiency of class switching. Patients typically have elevated levels of IgM and low or deficient levels of the other antibody classes.
Recurrent bacterial infections, particularly mucosal, are common.
How might an IgA deficiency present?
Patients with IgA deficiency have a predisposition to autoimmune disorders, mucosal infections, and atopic allergy.
What is antibody-mediated alteration of cellular function a mechanism/example of?
Give two examples
A type II non-cytotoxic hypersensitivity reaction.
Graves disease and Myasthenia gravis are examples.
What is antibody-mediated destruction of cells or tissues a mechanism/example of?
Give two examples
A type II cytotoxic hypersensitivity reaction.
Goodpasture disease and hemolytic disease of the newborn are examples
What is immune complex formation and deposition in tissues with complement activation a mechanism/example of?
Give two examples
This is the mechanism of a type III hypersensitivity reaction.
Two examples are: Rheumatoid arthritis and systemic lupus erythematosus
Goodpasture disease mechanism
autoantibodies against type IV collagen in the glomerular basement membrane
An example of type II hypersensitivity
Auto-antibodies against centromeres is associated with what disease?
Scleroderma (diffuse systemic sclerosis)
Systemic Lupus Erythematosus
Anti-RNPs (SS-A [Anti-Ro], SS-B [Anti-La])
Basic mechanism of Graves disease
This is an autoimmune disease that displays type II non-cytotoxic hypersensitivity. In this disease, antibodies are produced against the thyroid-stimulating hormone (TSH) receptor on the thyroid.
These antibodies are called long-acting thyroid stimulator (LATS)