Microbiology Ch 17

• Adaptive immunity - acquired
• - specific response to Ag with a Ab and lymphocytes

substance (protein or polysaccarides) that causes the body to produce Ag or sensitized T cells

• Ab = a protein made in response to an Ag
• specific Ab that can only combine with that Ag

Abs are a globulin class of protein (protein with globular form) so Ab are called immunoglobulins (Ig)

• 1. Cell mediated response (T cells)
• 2. Humoral response or antibody mediated - B cells & plasma cells (Abs)

• B cells = bursa derived (bursa of checken, not human)
• B cells arise from pluripotent cells that are produced and mature in the red bone marrow

B cell has specific Ag on it surface - when stimulated by matching Ag - it becomes a plasma cell - makes ↑# Abs (identical to Ab on B cell surface)

A plasma cell is a mature stimulated B cell that makes Abs

• Memory cells do not attack invaders - they remain in the system as
• clones (thousands) after a specific immune response - they speed up
• immune response is same Ag is encountered again in the future

• T cell = thymus derived
• - made in red bone marrow
• - mature in thymus (lymph tissue

Each has specific T cell receptor that binds to specific Ag - when Ag binds T cell is stimulated and produces cytokins → immune repsonse

Hapten = an small Ag molecule (too small to register respone) that contains an epitope - needs to be combined with a carrier protein to cause an immune response

2nd encounter - hapten alone will trigger immune response

• a. Cytotoxic T cells - CD8 (co-receptor)
• - activated by cytokins - cause apoptosis

• b. Helper T cells - CD4 (co-receptor)
• - release cytokins → activate dendritic cells (APCs), macrophages, cytotoxic T cells, B cells (plasma cells)

• c. Memory T cells - CD4 & CD8 (co-receptors)
• -
• d. Regulatory T cells - turn off specific immune response

Epitope = the part of an Ag that binds to the Ab and starts the immune response - also called an antigenic determinant

• CD4 T cells: -Exogenous Processing (MCH II/ Ag)
• 1. APC presents Ag to CD4 lymphocyte - Ag binds at TCR (T cell receptor) and CD4 is the coreceptor
• 2. Costimulant (such as IL-2) causes cell to become activated
• 3. CD4 T cells make active helper T cells - (they secrete cytokins (IL-2) and memory T cells - not active until next contact with Ag

• CD8 T cell - Endogenous processing (MCH I/ Ag)
• 1. APC presents Ag - Binds at TCR and CD8 is the coreceptor
• 2. Costimulator (possibly IL-2 secreted by activated CD4 cells) causes cell to be activated
• 3. Cell makes clones of active cytotoxic T cells - (attack invaders) and memory cytotoxic T cells - (can quickly activate and make active and
• memory cytotoxic T cells at next meeting of Ab)

• Complement and macrophages bind to the heavy chains on compliment.
• Ab monomer has a valence of 2

% = % of all Abs in serum

• 1. IgG (80%) - most abundant in blood - able to leave blood & migrate into tissue during immune response
• - monomer
• -triggers compliment when bound to Ag
• - increases phagocytosis (opsonization)
• - kills viruses & toxins
• - crosses placenta - innate immunity in fetus

• 2. IgM (7%) - large pentamer (M=macro)
• -1st Ab involved in immune respone -short life
• - triggers compliment
• -causes aggregation (valence 10)
• - serves as Ag receptor on surface of B cells - also found in blood in lymph

• 3. IgA (10%) - most abundant in body (not serum)
• - in secreations - mucous membranes - salvia, mucus, tears, milk
• - blocks adherance to membranes
• - dimer

4. IgD (.2%) - monomer - unknown function

• 5. IgE (.002%) - monomer -
• -serves as Ab receptor on Mast cells, basophils, eosinophils
• - particiapes in allergic reaction - in presence of allergen IgE stimulates the mast cell to release histamine
• - large #s during allergic reacion
• - involved in extracellular killing of large parasites

IgG

IgM

IgM, IgD

In secreations - saliva, milk, tears, mucus

• No unless having an allergic reaction - then lots
• Bound to Mast cells, basophuils, eosinophils that relase histomine in presence of allergen

• When an Ab/ Ag complex form Ab tabs microbe for death by:
• 1. aggluatination - clumping
• 2. opsonization - ↑ phagocytosis
• 3. activates compliment
• 4. cell mediated death (eosinophils → lytic enzymes)
• 5. neutralization of microbe - cant adhere

No it is a dimer

• 1. macrophages (A monocyte matures into a macrophage in tissue (not in blood stream)
• 2. neutrophils (PMNs)
• 3 .APCs - dendritic cells

In agglutination (also called aggregation) Ab cause Ag to clump together. IgM is very good at this becuase it has a valence of 10

• Ab mediated immune response occurs in the lymphoid tissue. T dependent Ags:
• 1. B cell eats Ag and is broken down into peptide fragments (combined with MHC-II) and moved to B cell plasma membrane
• 2. Helper T cell binds to B cell and costimulates - B cell divides into: Plasma cells & Memory B cells

• a. Specific B cell receptor (BCR) binds with an Ag
• b. The cell is now actived and undergoes clonal selection - plasma cells that secrete Ab and memory B cells for next encounter
• c. Plasma cells release thousands of Abs that travel in the lymph to site of infections

• T-independent Ags:
• Ags stimulate B cell directly-
• - provokes a weaker immune response
• - response is primarily IgM
• - no B membory cells are generated

Body dosent make Abs against itself

• all body cells (except RBCs) are tagged with MHC Ags
• -also called HLA Ags - Human leukocyte Ags
• - your body ignores there Ags

• After organ transplants the patient must take medication that inhibits
• immune response becuase the Ag on the new organ are foreign - the body
• will try to attack it. This is also a factor in autoimmune diseases
• where lymphocytes attack the bodys cells. However, it is not an issue
• in blood transfusion becuase the RBC do not carry MHC Ags - they only
• carry blood type Ags

Clonal selection = creating memory cells that are responsible for an enhanced secondary response to an Ag

Clonal deletion = removing all clones of B and T cells that are capable of damaging "self Ags"

Autoimmune diseases are those where cells arise that do not recogine "self Ags" are are able to damage body cells.

• A dendritic cell is a type of APC -it is nonspecific
• It is an agranulocyte derived from a moncyte
• -primary APC - engulf invader and take to T cells in the lymph

• Supress and inhibit other T cells
• - combat autoimmune disease by inhibiting T cells that escape deletion in the thymus
• - turn cell mediated immune reactions off using cytokins

• APC - Antigen Presenting Cell
• Dendritic Cells & Macrophages

• 1. They eat (phagocytosis) invaders
• 2. Attach a peptide fragment to their plasma membrane via MHC (major histocompatibility complex)
• 3. Travel to lymphatic tissue to present the antigen to T cells

• Natural killer cells (NK) are nonspecific lymphocytes -
• they can also attack parasite and tumors

Cytotoxic T cells leave lymphatic tissue and travel to infection - bind to cells with specific microbial Ags

• kills cell by one of several options:
• 1. can release granzymes - protein -digesting enzyme that trigger apoptosis (progranned cell death)
• 2. can release Perforin and granulysin
• - perforn makes hole in cell membrane (cell lysis) and granulysin enters cell through hole and kills microbe by creating holes in it cell membrane.
• 3. can release lymphotixin - activates enzymes in the target cell that cause the cells DNA to fragment (cell dies)

• Proteins- they mediate immune responses - produced by all cells of immune system in response to a stimulus
• -can stimulate or inhibit it
• -activate macrophages
• - transform B to plasma cells
• - transform B and T to memory cells

In Humoral response (B cell - Ab) - Helper T cell binds to B cell and releases cytokins to make B cell proliferate faster → plasma cells + memory B

• Examples:
• IL (interleukins), interferons, TNF tumor necrosis factor

• foreign Ags
• cytokins

Antibody-dependent cell-mediated cytotoxicity

• specific reaction Ab/Ag
• Extracellular killing - invaders that are too large to be phagotized - parasites

• 1. Parasite is coated with Ab
• 2. Macrophages attach to C regions of IgE & IgE can bind to eosinophil cell membrane
• Ag/IgE binding → enzymes released that digest parasite

• Ab titer - relative amt of Ab in the serum
• IgM - first Ab produced
• IgG - second Ab produced
• 

• Natural passive immunity - mother to fetus
• Natrual active immunity - infection Ab/Ag reaction
• Artificial active immunity - vaccination - inject Ag
• Artificial Passive immunity - inject Ab

• Blood serum with Ab against a certain Ags
• Injection can give immediate passive protection against the disease (that produced the Ags) - it does not last long (about 3 weeks)