unit 10 Flashcards
Antigen
- immunogen/ allergen/ AG
- usually proteins or large polysaccharides
- any substance that causes antibody formation
-can be a microbe
Antibody
-immunoglobulin, Ab, Ig
- protein made in response to an antigen
- binds to Antigen
Anitgen-antibody reaction
- antibody will attach to an antigen at a specific site
Valence
of Ag’s that will attach to an Ab
Types of accquired immunity
passive and active
active accquired immunity
- natural active and artificial active
natural active immunity
- come across antigen naturally
- ex= cold viruses
artificial active immunity
- antigen artificially introduced (vaccine)
- Hib MMR Dtap
Natural passive immunity
-Ab goes from mother -> infant
-placental or colostrum
Colostrum
first breast milk when baby is born
Artificial passive immunity
- Ab recieved via injection
-ex= antitoxins or rhogam ( anti-RH antisera)
Serum immunoglobulins
IgA
IgD
IgE
IgG
IgM
IgA
- secretory Ab
- 70,000 or 400,000 Daltons
-found in mucous, saliva , tears, colostrum, blood - 1st / 3rd line of defense
-monomer in blood, dimer in secretions
IgD
-180,000 daltons
- internal marker on B cells
-monomer
- sticks to lymphatic b cells
IgE
- 200,00 daltons
-allergic Ab - involved in allergic reactions/ hypersensitivity
- monomer
-least abundant Ab
IgG
- circulatory Ab
- 160,000 daltons
- protects against microbes
-triggers complements - increases phagocytosis
- crosses fetal- placental membrane
- monomer
-most abundant Ab
What special about IgG
first antibody to increase at first antigenic response
IgM
-circulatory Ab
- 900,000 Ab
- 1st Ab to arrive in response to initial exposure to Ag
-short lived
- does not cross fetal-placental membrane
-Pentamer
anamnestic response (antibody memory)
initial = 4->7 days (IgM) 10 -> 17 days (IgG)
Secondary = 2 -> 7 days (IgG) with greater magnitude
Does an antibody destroy an antigen
no
Antibody structure of a monomer
- 4 polypeptide chains (2 heavy 2 light)
- joined by disulfide bonds to form a Y shape
Arms of Y (Fab region -fragment of antigen binding)
- region where Ag binds
-has variable amino acid sequence - specific for Ag
Stem of Y (FC region - fragment of cell binding)
-has constant amino acid sequence
- binds to cells , proteins, complements
Which Ab are monomers?
IgA (monomer in blood , dimer in secretions)
IgD
IgE
IgG
T cells and cellular immunity
- produced by stem cells in red bone marrow
- matures in thymus
- makes up 65% of lymphocytes
- responds to ags
- secrete cytokines
what are cytokines
chemical messengers
Types of T cells
T helper cells
Regulatory T cells
Cytotoxic cells
T helper cells
- cd4 cells
- activates B cells to make Abs/ macrophages
- secretes cytokines
Regulatory T cells
= suppressor = cd8 cells
- suppresses other T cells
-protects fetus from rejecting body cells
Cytotoxic Cells
- cd8 cells
- recognize/ kill target cells
- non self or hijakced cells
- programmed cell death (apoptosis)
- not capable of attaching to helper cells
Cytokines
- chemical messengers of immune cells
-also known as interleukins / interferon - more than 200 types
- attracts macrophages/ protects against viral infections
- toxic to tumor cells
-increases Ab production - sends info -> host cell about foreign material
B cells and humoral immunity
-produced by stem cells
-matures in bone marrow
- makes up 35% of lymphocytes
- primarily found in blood/ lymphoid organs
function of B cells
- carry old immunoglobbulins (IgD or Igm) on surface
- when they recognize an Ag, the B cell is activated with the assistance of T cells to produce memory cells/ plasma cells
Memory cells ( B cell)
- stores info based on specific amino acid sequence
plasma cells (b cell)
produce new Ab’s
Results of antigen-antibody binding
1) when Ab encounters specific Ag / it forms an Ag-AB complex form
2) Ab molecule is not damaging to Ag but it triggers mechanisms that are
3) types of mechanisms
- aggulutination
- Opsonization
- Neutrilization
- Complement activation
Aggulination
reduces number of microbes
Opsonization
enhances phagocytosis
Neutralization
blocks viral attachment/ neutrilizes toxins
Complement activation
serum protein that causes inflammation/ cell lysis
Congenital immunodeficiencies
SCID
Bruton’s disease
DiGeorge syndrome
SCID - severe combined immunodefiency (congenital immunodefiency)
- deficiency in both T/ B cells
- no Ab’s
- treatment = gene therapy/ restriction enzymes
- rare
Bruton’s disease
- decrease # of B cells
- less Ab’s
- more prone to infections
DiGeorge Syndrome
-Defective thymus (Less T cells)
- more prone to infections
Autoimmune disease
- Ab against itself
- rheumatoid arthritis (anti gammaglobulin Ab’s)
- Systemic Lupus Erythematosus (anti-dna Ab’s)
AID’s acquired immunodefiency syndrome
- HIV attaches to cd4 receptors on T helper cells
-decreased # of T helper cells - normal levels of B cells
- B cells not turned on because of lack of T helper cells (decreased # of Ab’s)
Graft
transfer of tissue from one part of the body to another or from one person to another
Autograft
tissue graft from oneself
Isograft
tissue graft from an identical twin
Allograft (homograft)
transfer of graft from one person to another person of the same species
Xenograft
tissue graft from different species
Immediate or Antibody Mediated
1) Type I : Anaphylactic reaction
2) Type II: Cytotoxic reaction
3) Type III: Immune complex reaction
Delayed or cell mediated
Type IV: delayed type reaction (T helper cell usually delayed)
Type I: Anaphylactic reaction
- ex = insect stings / drug or food allergies / hay fever/ allergic asthma
- 2-> 30 minutes
- 1st exposure to allergen
Sensitizing dose: 1st exposure of Type I
produces IgE: Fab recognizes allergen and Fc attaches to basophils or mast cells
Shocking dose: 2nd exposure of Type I
- basophils/ mast cells increase result in histamines increasing
- gastric, lacrimal, and nasal secretions
- vascular permeability increase
- BP decreases resulting anaphylactic shock
- localized hives/ itching/ reddening
Treatment for Anaphylactic reaction
Anti-histamine or epinephrine (constrict blood vessels/ increases BP)
Lab tests for Anaphylactic reaction
skin test Eosinophilia IgE (Rast)
Type II: Cytotoxic reaction
- examples = transfusion blood reactions, hemolytic disease of newborn
- 5 -> 12 hrs
- body exposed to Ag/ attaches to target cells (rbc, wbc, platelets)
- complement activated / cytolysis occurs
Type III: Immune complex reaction
-Examples = post-streptococcal / Glmerulonephritis / Rheumatic fever
- sequelae infection : secondary consquence
- 3 -> 8 hrs
- Body exposed to Ag , makes IgG or IgM Ab
- Ab binds with Ag and forms Ab-Ag immune complex
IC’s
what are IC’s
- deposits on blood vessel walls
- penetrates walls to cause inflammation
Type IV: Delayed type hypersensitivity reaction
-Examples = TB Tine skin test / some drug allergies / poison ivy
- 2 -> 3 days ( due to time for T cells/ macrophages -> Ag)
- No Ab involvement; caused by T cells
Purpose of Type IV: delayed type hypersensitivity reaction
- Ag -> body and attaches to target tissue (skin)
- T cells react with Ag to destroy Ag but it also destroys target tissue (dermatitis)
