Adaptive Immunity Ch 9 Flashcards
Types of adaptive immunity (2)
Acquired (active) and passive
Innnate versus adaptive immunity
Innate- non specific response, generalized, always responds
Adaptive- specific to invading organism, antibodies are specific providing long term protection and memory
antigen
The invader (bacteria, fungi, viruses, allergens, self)
Haptens
Too small alone to be immunogenic but binds with larger protein molecules to create response ie PCN, poison ivy
Antibody (Ig)
Short term versus long term immunoglobulins
Short- IgM is the first to respond, IgA (innate), IgE (allergy)
Long term IgG
IgD less known about
Antigen presenting cells
Lymphocytes cannot identify antigens by themselves the antigen presenting cell process (detects and engulf) and present the antigen for recognition by the T cells to activate the acquired response
Dendritic for new
Macrophage for old
4 categories of T cells
Memory T cells, helper T cells, regulatory T cells, cytotoxic T cells
Memory T cells
(CD 2) located on cell surface and work as marker for T cells
Helper T cells
(CD4) assist in activation in CD8, NK cells, B cells
Regulatory T cells
(CD4) help prevent autoimmune response
Cytotoxic T cells
(CD8) binds to surface antigen and destroys infected cells
T cell mature in the
Thymus, 2 chains join to make 1 specific antigen receptor
T cells provide this type of immunity
Cellular
How do T cells respond to antigens
Slower, stimulate cytokine response to activate leukocyte response or kill target activity
T cells maturity results in
Decrease response, no antibodies developed
Problems if T cells are impair
Opportunistic infections
B cell mature here
Bone marrow, some will turn into memory cells
B cell immunity type
Humoral
B cell response to antigen
Have antigen binding sites with 2 roles once activated it produces daughter cells that make plasma cells. These cells are the antibody factories, and they secret IgM specific to antigens. Work outside the cell, bind and neutralize, secrete antibodies to fight antigens
B cell antibody production
Initial exposure- IgM production 7 days post exposure, IgG production makes 75% of antibodies , then levels drop
Secondary exposure- increase in IgG rapid, large amounts and remains elevated
B cell maturity results
Quicker response
B cell issues if impaired
More systemic reactions and more susceptible to encapsulated organisms
4 ways antibodies provide protection from antigens
Neutralization
Opsonization
Agglutination
Precipitation
Neutralization
Inactivate or cover the toxic portion of the antigen
Opsonization
Make antigen more identifiable for phagocytosis
Agglutination
Causes antigens to clump together and make it easier to eradicate one big group instead of many separate
Precipitation
Dissolve antigen into a solid
Direct effects on an antigen
Cover receptor sites to prevent antigen attachment like in an attenuated virus
Bind with a toxin and neutralize it like in tetanus toxoid
Indirect effects in antigen
Antibodies activate the innate immune system, complement and phagocytosis, IgM complement activation, IgA Opsonization
Acquire adaptive immunity
After exposure to antigen or immunization, requires host immune system to respond, generate long term immunity
Ex, chicken pox, measles, Covid
Infection or vaccination
Passive adaptive immunity
Antibodies or T cells are transferred to recipient from donor
No immune response from host
Only temporary protection
Ex. Maternal antibodies, rabies
Process of presenting and packaging the antigen for the lymphocytes
Macrophages role if it is a known antigen
Dendritic cells if naive antigen
Lymphocytes in waiting
T cells produced in the thymus
B cells in the bone marrows
Move to secondary lymphoid cells as their waiting room lymph, spleen, tonsil, adenoids, Peyer patch, appendix
Aspects that affect the immune system
Stress-decrease number of lymphocytes
Nutrition- decrease in zinc, B12, A, C, E, decrease B and T cell function and complement activation
Cancer- cytokines-damage cells around CA, risk of nutrition deficiency
Immunosuppressive- targets CA cells and healthy cells, opportunistic infections
Immune hypersensitivities (3)
1- allergy
3-immune complex hypersensitivity, AKA autoimmune
4-cell mediated AKA graft v host disease
Type 1 hypersensitivity (allergy)
Caused by mast cells, IgE
Antigen degranulation results in histamine release, basophils and eosinophils respond, systemic vasodilation, and drop in BP
Bronchoconstriction, respiratory distress, increase in vascular permeability
TX is epi
Type 3 hypersensitivity immune complex hypersensitivity
Anti DNA, immune complexes to own DNA, antigen antibody complexes present to tissue, complement activated, neutrophils are notable to phagocytize lysosome into the tissue, test by anti nuclear antibodies (ANA)
Affect kidneys, connective tissue, heart, Brain, damage is progression
No cure, TX symptoms-anti inflammatory, IVIG, methotrexate
Type 4 hypersensitivity cell mediated
Cel mediated if HLA doesn’t match enough,, t helper, cytokines, macrophages, cytotoxicosis, kill target cell if can’t be killed may be walled off with a granuloma
Graft V host disease, will attack transplanted tissue
TX is anti rejection drugs and steroids
Immune related changes in newborns/fetus
Maternal antibodies start to transfer to placenta in the 1st trimester, and stop at about 37-40 weeks, preterm babies at risk for infection, last about 6 months PP, T and B cell production starts at 6-8 months PP, weak immune system, less mature, can get IgA, IgG, IgM from breast milk
Age related immune changes in the elderly
Decrease in number of T cells, B cells less responsive, decreased memory, “inflammaging” chronic inflammation r/t aging that results in chronic illness
Secretory immune response
Systemic immune response in the mucosal system such as lacrimal, salivary, bronchial, breast, GI, GU glands/tissue
Plasma cells in secretory organs produce antibodies in secretions, these antibodies are secreted and act locally, IgA most common
Major histocompatibility complex
All cells (except RBC) have glycoprotein markers on the surface, genetic MHC loci inherited one from each parent. Combination off MCH marker play a role in human leukocyte antigen (HLA type). 6 basic types with 150 different variations, when one of these antigens is not present an individual may develop antibodies to it on exposure-causing transplant rejection
Secondary role in controlling quality and quantity of immune response
