From Innate to Adaptive Immunity II Flashcards

1
Q

Where do T lymphocytes develop?

A

begin their development in the bone marrow, but mature in the THYMUS

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2
Q

what are the 2 main classes of T cells?

A

Helper T cells (with 5 subtypes) and Cytotoxic/Killer T cells

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3
Q

What is the T cells’ principle role in immunity?

A

T lymphocytes recognize and remove foreign substances. T cells themselves survey the surfaces of the body’s cells, looking for ones that have parasites within them or that are dangerously mutated. T cells recognize antigens by means of their surface receptors which see antigens presented by the newly arrived dendritic cell that is traveling via lymphatics to a lymph node (antigen has been partially digested by DC and peptides derived from it are loaded into special antigen-presenting molecules called MHC Class II and go to cell surface).

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4
Q

When helper T cell receptor recognizes foreign material, it

A

becomes activated, proliferates and the daughter cells travel through the body until they reach where the antigen first invaded. They are then re-stimulated by local antigen-presenting cells and release short-range mediators called lymphokines (cytokines made by lymphocyte). These mediators call up a much augmented inflammatory response by attracting monocytes and macrophages (specialists in phagocytosis and destruction).

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5
Q

Cytotoxic T cells “killers” also

A

examine surface of incoming DCs but they are looking for fragments on a different class of antigen-presenting molecule, MHC Class I, which is on ALL CELLS. Appropriate clones of cytotoxic T cells proliferate and daughter cells circulate. When daughter cell binds a cell showing the same peptide it delivers a lethal “hit” signaling target cell to commit suicide (apoptosis).

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6
Q

What is a fully differentiated B cell called and what does it do?

A

a plasma cell and is an antibody production factory

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7
Q

Discuss in principle the role B cells play in immunity

A
  • B cells also recognize and remove foreign substances, but B cells protect the extracellular spaces of the body (tissues fluids, blood, secretions), by releasing antibodies into these fluids.
  • B cells also arrange for phagocytosis and destruction of foreign material, they recognize antigens via surface receptors and become activated and proliferate (they DO NOT require the simultaneous recognition of an associated MHC molecule—like T cells). Then, they release soluble versions of their receptors (antibodies) which go and do the work
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8
Q

Chief function of Immunoblobin G (IgG):

A

most abundant antibody, 2 adjacent IgG molecules binding an antigen cooperate to activate COMPLEMENT, a system of proteins that enhances inflammation and pathogen destruction. Only antibody that passes mother to fetus, so its important in protecting newborn until it can get its own IgG synthesis

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9
Q

Chief function of Immunoblobin M (IgM):

A

Better at activating COMPLEMENT system than IgG, first antibody to appear in blood after exposure to new antigen. Replaced by IgG in 1-2 weeks

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10
Q

Chief function of Immunoblobin D (IgD):

A

antibody inserted into B cell membranes as their antigen receptor

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11
Q

Chief function of Immunoblobin A (IgA):

A

most important antibody in secretions (tears, saliva, intestinal fluid and milk). Associated with SECRETORY COMPONENT—makes antibody resistant to digestive enzymes and plays a role as the first line of defense against microorganisms

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12
Q

Chief function of Immunoblobin E (IgE):

A

designed to attached to mast cells in tissues. Once attached, when it encounters antigen, it will cause the mast cell to make prostaglandins, leukotrienes and cytokines and release its granules which contain mediators of inflammation (like histamine). Real role: resistance to parasites like worms.

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13
Q

Type I Immunopathology (what is it, who has it)

A

immediate hypersensitivity: Patient makes too much IgE to environmental antigen (pollen or food). 10% of population has allergic symptoms

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14
Q

Type II Immunopathology (what is it, how to treat)

A

autoimmunity due to antibodies which react against self: This can happen if foreign antigen looks like “self” molecule;
Treat these diseases with immunosuppressives and anti-inflammatory drugs

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15
Q

Type III Immunopathology (What is it, symptoms, Diseases, what causes it)

A
  • When patient makes antibody against a soluble antigen: Antigen-antibody complex is usually eaten, but if they are too small, they may get trapped in basement membrane of capillaries they circulate through. Trapped complex activated COMPLEMENT and inflammation occurs.
  • Symptoms: arthritis, glomerulonephritis, rash, pleurisy.
  • Diseases: systemic lupus erythemtosus and rheumatoid arthritis.
  • Foreign antigens that cause Type III: penicillin (in large doses) and foreign serum, “serum sickness”.
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16
Q

Type IV Immunopathology (what is it, example)

A

T-cell mediated: Can be autoimmune or innocent bystander disease. Example: in TB most of the cavity formation in lungs is T cell mediated, not bacterium mediated (they are just doing their job).

17
Q

Chronic frustrated immune responses (what is it and example)

A

Antigen is not “self” but is something you can’t get rid of, ie: gut bacteria (inflammatory bowel disease) OR gluten (celiac disease).

18
Q

AIDS (what is it caused by and what does it do)

A

Caused by HIV-1 infection of the TH cells (binds to the CD4 molecules they have on their surface). Inside, it uses reverse transcriptase, to copy RNA to DNA and inserts its DNA into host cell. Remains latent until reactivated when the T cell is activated by antigen, leading to progressive loss of Th cells

19
Q

Examples of immunopathology (6)

A

Type I-IV immunopathology, chronic frustrated immune responses and AIDS