CHAPTER 4- IMMUNOLOGY
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T cells :
- 1) thymus
- 2) cell mediated
- 1) release IL-4 (most potent), which causes B-cell maturation into plasma cells2) release IL-2 (most potent), which causes maturation of cytotoxic T cells
- 3) Involved in delayed-type hypersensitivity (brings inflammatory cells by chemokine secretion)
- 4) Th1 helper T cells:
- 1- predominant release of pro-inflammatory cytokines (IL2, IFN-gamma)
- 2- involved in cell-mediated responses
- 5) Th2 helper T cells1- predominant release of anti-inflammatory cytokines (IL-4--> inhibits macrophages)
- 2- involved in atopy and allergic responses
Suppressor T cells (CD8)
regulate CD4 and CD8 cells
Cytotoxic T cells (CD8)
recognize and attack non-self-antigens attached to MHC class I receptors (i.e. viral gene products)
Intradermal skin test (i.e. TB skin test)-
used to test cell-mediated immunity
Infections associated with defects in cell-mediated immunity
intracellular pathogens (TB, viruses)
What can increase T-cell-mediated immunity?
See image on pg 16: T-and B-cell activation:
Two signals are required. First, alloantigen binds to antigen-specific receptors- the TCR (T cells) or surface IgM (B cells). The second, or costimulatory, signal is provided by IL-1 released by the antigen-presenting cell. CD4 helper T cells (Th) release IL-2, IL-4, and IL-5, which provide help for CD81 T cells (Tc) and for B-cell activation.
- 1) bone
- 2) antibody-mediated (humoral) immunity
- 3) IL-4 from helper T-cells stimulates B cells to become plasma cells (antibody secreting)
MHC class I:
- 1) A, B, C
- 2) CD8 cell activation
- 3) present on all nucleated cells
- 4) single chain with 5 domains
- 5) target for cytotoxic T cells
MHC class II
- 1) DP, DQ, DR
- 2) CD4 cell activation
- 3) present on B cells, dendrites, monocytes, and antigen-presenting cells
- 4) 2 chains with 4 domains each
- 5) activator for helper T cells
- 6) stimulate antibody formation
- 1) endogenous viral proteins produced, are bound to class I MHC
- 2) go to cell surface, and are recognized by CD8 cytotoxic T cells
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
These pathways are the general mechanisms by which viral and bacterial infections are handled. There are some examples of crossover between MHC class I and class II immunity, meaning viruses get presented through MHC II pathway and bacteria through MHC I pathway.
See picture on Pg. 17: Antigen processing and presentation.
Endogenously snythesized or intracellular proteins are degraded into peptides that are transported to the ER. These peptides bind to class I MHC molecules and are transported to the surface of the antigen-presenting cell.
CD8+ cells recognize the foreign peptide bound to class I MHC by way of the TCR complex. Exogenous antigen is endocytosed and broken down into peptide fragments in endosomes. Class II molecules are transported to the endosome in association with the invariant chain, bind the peptide, and are delivered to the surface of the antigen presenting cell, where they are recognized by CD4+ cells.
Natural Killer Cells:
- 1) not restricted by MHC
- 2) do not require previous exposure
- 3) do not require antigen presentation
- 4) not considered T or B cells
- 5) recognize cells that lack self-MHC6) part of the body's natural immunosurveillance for cancer
- 1) initial antibody made after exposure to antigen
- 2) is the largest antibody, having 5 domains (10 binding sites
- 1) most abundant antibody in body
- 2) responsible for secondary immune response.
- 3) can cross the placenta and provides protection in newborn period
- 1) found in secretions
- 2) in peyer's patches in gut
- 3) in breast milk (additional source of immunity in newborn)
- 4) helps prevent microbial adherence and invasion in gut
membrane-bound receptor on B cells (serves as an antigen receptor)
- 1) allergic reactions
- 2) parasite infections
Which antibodies are opsonins?
Which fix complement?
- IgM and IgG are opsonins
- IgM and IgG fix complement (requires 2 IgGs or 1 IgM)
What region of the antibody recognizes antigen?
Which region of the antibody is recognized by PMNs and macrophages?
- 1) constant region
- 2) Fc fragment does not carry variable region
have multiple binding sites to the antigen and multiple epitopes
have only 1 binding site to 1 epitope
Whats the major source of histamine in the blood?
Whats the major source of histamine in tissue (other than stomach)?
Primary lymphoid organs:
- 1) liver
- 2) bone
- 3) thymus
Secondary lymphoid organs:
2 different cell lines in one individual (bone marrow transplant patients)
- 1) converts lymphocytes to lymphokine-activated killer (LAK) cells by enhancing their immune response to tumor
- 2) also converts lymphocytes into tumor-infiltrating lymphocytes (TILs)
- 3) has been shown to be successful for melanoma
How do you treat non-tetanus-prone wounds:
1) give tetanus toxoid only if patient has received <3 doses or tetanus status unknown
How do you treat tetanus prone wounds?
1) <6 hours old; obvious contamination and devitalized tissue; (crush, burn, frostbite, or missile injuries)- always give tetanus toxoid unless patient has had >3 doses and its has been <5 years since last booster
When do you give tetanus immune globulin?
give only to patient with tetanus-prone wounds who have not been immunized or if immunization status unknown
Type I hypersensitivity:
- Type I:
- Immediate hypersensitivity reaction (allergic reaction) IgE mediated: mast and basophils release histamine, serotonin, and bradykinin in response to release of major basic protein from eospinophils, which have IgE receptors of the antigen
Examples: bee stings, peanuts, hay fever
Type II hypersensitivity:
IgG or IgM reacts with cell-bound antigen
- ABO blood type incompatibility, Rh incompatibility, Graves disease, myasthenia gravis, ITP
Type III hypersensitivity:
Immune complex deposition
Examples: serum sickness, rheumatoid arthritis, SLE
Type IV hypersensitivity:
- Delayed-type hypersenstivitiy
- Antigen stimulation of previously sensitized T cells
Examples: TB skin test, contact dermatitis
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