Chapter 4: Immunology Flashcards
- Release IL-2 (causes maturation of cytotoxic T cells)
- Release IL-4 (causes B-cell maturation into plasma cells)
- Involved in delayed-type hypersensitivity
Helper T cells (CD4)
Causes maturation of cytotoxic T cells
IL-2
Causes B-cell maturation into plasma cells
IL-4
Brings in inflammatory cells by chemokine secretion
Delayed-type hypersensitivity
Regulate CD4 and CD8 cells
Suppressor T cells (CD8)
Recognize and attack non-self-antigens attached to MHC class 1 receptors (e.g. viral gene productS)
Cytotoxic T cells (CD8)
Used to test cell-mediated immunity
Intradermal skin test (i.e., TB skin test)
Infections associated with defects in cell-mediated immunity
Intracellular pathogens (TB, viruses)
- CD8 cell activation
- Present on all nucleated cells
- Single chain with 5 domains
- Target for cytotoxic T cells (binds T cell receptor)
MHC class 1 (A, B, C)
- CD4 cell activation
- Present on antigen-presenting cells (e.g., monocytes, dendrites)
- 2 chains with 4 domains each
- Activates helper T cells (binds T cell receptor)
- Stimulates antibody formation after interaction with B cell surface IgM
MHC class II (DR, DP, and DQ)
Mechanism of immune response to viral infection
Endogenous viral proteins are produced, are bound to class I MHC, go to cell surface, and are recognized by CD8 cytotoxic T cells
Mechanism of immune response to bacterial infection
Endocytosis, proteins get bound to Class II MHC molecules, go to cell surface, recognized by CD4 helper T cells -> B cells which have already bound to the antigen are then activated by the CD4 helper T cells; they then produce the antibody to that antigen and are transformed to plasma cells and memory B cells.
- Not restricted by MHC, do not require previous exposure, do not require antigen presentation
- Not considered T or B cells
- Recognize cells that lack self-MHC
- Part of the body’s natural immunosurveillance for cancer
Natural Killer Cells
Initial antibody made after exposure to antigen. It is the largest antibody, having 5 domains (10 binding sites)
IgM
Most abundant antibody in body.
Responsible for secondary immune response.
Can cross the placenta and provide protection in newborn period.
IgG.
What type of cells do natural killer cells recognize?
Recognize cells that lack self-MHC
Two signals that cause activation of T and B cells
- Alloantigen binds to antigen specific receptors. (TCR - T cells; IgM - B cells)
- IL-1 release by APC.
CD4 helper T cells release IL-2/4 which provide help for CD8 T cells and B-cell activation.
Endogenous antigen processing and presentation
Endogenous proteins are degraded into peptides that are transported to ER. Peptides bind to MHC-1 and transported to surface of APC. CD8 cells recognize complex by way of TCR complex.
Exogenous antigen processing and presentation
Exogenous antigen is broken down into peptide fragments in endosomes. Class-2 molecules transport to endosome, bind the peptide, and delivered to surface of APC cell, where they are recognized by CD4+ cells.
Found in secretions, in Peyer’s patches in gut, and in breast milk (additional source of immunity in newborn); helps prevent microbial adherence and invasion in gut.
IgA
Membrane-bound receptor on B cells (serves as an antigen receptor)
IgD
Allergic reactions, parasite infections
IgE
Opsonins
IgM, IgG
Fix complement
IgM, IgG (requires 2 IgGs, or 1 IgM)
Region: antigen recognition
Variable region
Region: recognized by PMNs and macrophages.
Constant region
Fragment that does not carry a variable region
Fc fragment
Have multiple binding sites to the antigen at multiple epitopes
Polyclonal antibodies
Have only 1 binding site to 1 epitope
Monoclonal antibodies
Immediate hypersensitivity reaction (allergic reaction) eosinophils have IgE receptors for the antigen and release major basic protein, which in turn activates mast cells and basophils, which release histamine, serotonin and bradykinin
Type 1
Ex: bee stings, peanuts, hay fever
Hypersensitivity: IgG or IgM reacts with cell-bound antigen
Type 2:
Ex: ABO blood incompatibility, Graves’ disease, myasthenia gravis
Hypersensitivity: Immune complex deposition
Type 3
Ex: Serum sickness, SLE
Hypersensitivity: Delayed-type hypersensitivity - antigen stimulation of previously sensitized T cells
Type 4
Ex: TB sin test (PPD), contact dermatitis
Major source of histamine in the blood
Basophils
Major source of histamine in tissue
Mast cells
Primary lymphoid organs
Liver, bone, thymus
Secondary lymphoid organs
Spleen and lymph nodes
2 different cell lines in one individual (e.g., bone marrow transplant patients)
Immunologic chimera
- Converts lymphocytes to lymphokine-activated killer (LAK) cells by enhancing their immune response to tumor.
- Also converts lymphocytes into tumor-infiltrating lymphocytes (TILs)
- Has shown some success for melanoma
IL-2
What two cells does IL-2 convert lymphocytes into?
Lymphokine-activated killer (LAK) cells and tumor-infiltrating lymphocytes (TILs)
When do you give tetanus toxoid to non-tetanus prone wounds?
Give tetanus toxoid only if patient has received
When do you give tetanus toxoid to tetanus-prone wounds?
Always give tetanus toxoid unless the patient has had > 3 doses and it has been
Criteria for tetanus-prone wounds
> 6 hours old. Obvious contamination and devitalized tissue. Crush. Burn. Frostbite. Missile injuries.
When would you give tetanus immune globulin with tetanus prone wounds?
Give only with tetanus-prone wounds in patients who have not been immunized or if immunization status is unknown.
