Adaptive Body Defense (415-427)
Overview
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Works against abnormal body cells and pathogens  when fails cancer AIDS
When the immune system responds to a pathogen  immune response… includes
o Increased non-specific defenses like the inflammatory response, fever, etc
o Cells that target specific antigens
Once you’ve met an antigen you don’t forget it & body will react faster and more intensely to the
same antigen next time  b/c you have antibodies (proteins that work against the same
pathogen)
If you inject a solution w/ antibodies into someone who has not been exposed to the actual
pathogen, they MAY be protected
3 key aspects about adaptive defense:
o It’s antigen specific- works against specific pathogens
o It’s systemic- not limited to a single portion of the body
o It has a memory- recognizes and attacks “old enemies” stronger
Learned if you inject the actual lymphocytes from one person into another then you’re protected
2 parts
o Humoral immunity “antibody-mediated immunity”
 Uses antibody in bodily fluids
o Cellular immunity “cell-mediated immunity”
 When lymphocytes protect the body (direct by lysing or indirect by releasing
chemicals to start the immune response or activate other immune cells)
 Has cellular targets  cancer cells, virus-infected tissue cells, cells of foreign origin
Antigens (Ag)
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Any substance that initiates an immune response
Large, complex molecules not normally in body
“non-self” substances (can be foreign proteins, nucleic acids, large carbs, some lipids)
Strongest antigens are proteins
Microorganisms are recognized as antigens b/c they have foreign molecules on their surfaces
Our cells are coated with many proteins “self-antigens”
o As our IS develops it learns to recognize the proteins as self
o While these are safe in our bodies when they are seen as antigens and cause an IS
 Why people w/ organ transplants & skin grafts need to take drugs to cripple the
immune response
Usually small molecules are not recognized as antigens but if they attach to our own proteins they
IS may recognize the combination of molecules as foreign and attack  can be harmful (allergies
o Will be discussed later
o Small molecule that bind to your proteins and cause an immune response  hapten “to
grasp” or an incomplete antigen
 Haptens are in drugs (penicillin) and chemicals found in poison ivy, pet dander,
detergents, make up, etc
Cells of the Adaptive Defense System
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Crucial cells
o Lymphocytes  work on specific antigens
 B lymphocytes (B cells)- make antibodies and oversee humoral response
 T lymphocytes (T cells)- no antibodies, run the cell-mediated part of the defense
system
o Macrophages  DON’T work on specific antigens but help lymphocytes that do
i. Lymphocytes (WBC):
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o Made in hemocytoblasts of red bone marrow
o Immature lymphocytes are pretty identical, T or B determination depends on where it
develops into an immunocompetent cell (where it becomes able to respond to a specific
antigen)
 T cells  thymus  go to lymph nodes & spleen to go to work go to lymph nodes
& spleen to go to work to reach full maturation
 Mature for 2-3 days, development is regulated by thymic hormones
 When immature lymphocytes get there, they divide so there’s a large # BUT
only T cells best able to ID antigens survive
o T cells that react to your “self proteins” and attack “self cells” are
destroyed
o HENCE the development of self-tolerance for you own cells
 B cells  bone marrow  go to lymph nodes & spleen to go to work to reach full
maturation
 Less is known about how they mature
o B cells that react to your “self proteins” and attack “self cells” are
destroyed
o When immunocompetent the T or B cell can react to 1 antigen only b/c all cell receptors
on B or T cell’s external surface are the same
 Receptors of one lymphocyte recognize only hepatitis A virus or only the
pneumonia-causing bacteria
Lymphocytes circulate through out body via blood and lymph to find invaders
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***ARE CERTAIN lymphocytes become immunocompetent before they meet antigens they
respond to THUS our genes, NOT antigens, determine what foreign substances our IS will be able
to recognize
Only some antigens our bodies “know” to resist will get into our systems, some lymphocytes
never get to go to work
Macrophages “Big eaters” and “antigen presenters”
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Widely distributed through out lymphoid organs and connective tissue
Come from monocytes made in the bone marrow
To work engulf a foreign substance AND present fragments of the antigens on their own surface
Release cytokines (chemical)
o Proteins used in immune response to attract WBC to injured area
o Keeps macrophages in the injured area or area where pathogens have been identified
o A lot of functions!
Then immunocompetent T cells come in and release chemicals that inc the macrophages appetite
so now it’s called a killer macrophage
***macrophages are not specific BUT they help the lymphocytes that are specific
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Usually remain in lymphoid organs
Humoral Immune Response (Antibody-Mediated)
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An immunocompentent but not yet mature B cell fully matures when antigens bind to its surface
receptors
Binding event activates B cell (T cells play a role too, discussed later) to undergo clonal selection
(lymphocyte grows and multiplies) to make an army of identical B cells w/ same antigen-specific
receptors
All identical cells made from the same original B cell are a family  called a clone
Clone formation is the primary humoral response to the specific antigen
Most members of the clone family become plasma cells “antibody making machines” (produce
2000 antibodies/sec)
o B cells make antibodies but not as much
Plasma cells live for 4-5 days then begin to die
During primary response antibody levels in the blood peak about 10 days after the immune
response begins then antibodies decline
B cells that don’t become plasma cells become memory B cells “immune system’s memory”
can respond to the same antigen during a later meeting now called the secondary humoral
response
Secondary humoral responses are:
o Faster
o More prolonged
o More effective
o Within hours of recognizing an “old” antigen/enemy, new plasma cells are being made
causing antibodies to flood the blood stream --? Within 2-3 days antibody levels peak at
higher levels than seen in the primary humoral response and the levels remain high for
weeks-months
Active & Passive Immunity
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Active immunity- when B cells meet antigens and produce antibodies against them; is:
o Naturally acquired- when we become infected with viruses and bacteria some of which
cause us to become sick and develop symptoms of their presence
 Active- we get infected by a pathogen (in immunological memory)
 Passive- antibodies pass from mom to child via placenta or breast milk (short term,
several months)
o Artificially acquired- we’re given a vaccine
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Active- give vaccine of dead or attenuated/living but weakened pathogens (in
immunological memory)
 Passive- injected w immune serum (gamma globulin) (short term, 2-3 weeks)
Vaccine are beneficial b/c we:
o don’t get as sick as with vaccine’s presence as we would upon initial exposure to actual
pathogen (lessened signs and symptoms) during the primary response
o Weak antigens produce an immune response so the body “remembers” the pathogen so
when see it for real we go to the secondary response
o PURPOSE OF A BOOSTER SHOT? (may intensify immune reponse when meet pathogen
later)
Passive Immunity- diff. from active an far as antibody source and degree of protection
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o B cells do NOT produce the antibodies, they exist in the serum from an immune human or
animal donor  no memory B cells are made
o Gamma globin given after exposure to hepatitis
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o Immune sera are given for rabies, snake, bites, botulism, and tetanus b/c the diseases will
kill you before you can build active immunity
Monoclonal antibodes used in cancer/drug research, diagnose pregnancy, dx rabies,& dx hepatitis
Antibodies AKA Immunoglobuluns (Ig)
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Make gamma globulin part of blood proteins
Proteins, made by B cells or plasma cells offspring when activated by antigens
Bind to specific antigens
Share similar basic anatomy
o Consist of 4 peptide chains bonded together by disulfide bonds (where S-S) to make
symmetrical sides
o 2/4 chains are identical, ~400 amino acids each heavy chains
o Other 2 are identical, 12 as long  light chains
o Have variable region at one end that make unique antigen binding sites (2 sites/antibody)
o Have larger constant region at other end, has common function for all antibodies BUT are
slightly different and used to determine antibody type/class, how antibody class will
perform its immune roles, cell types/chemicals that antibody can bind to
Formed b/c of many different antigens so all have unique shapes/qualities (are 5 Ig classes w/
different structures and function) MADGE
o IgD, IgG, IgE  share basic Y shape, monomers
o IgA  can be monomers or dimmers (2 linked monomers)
o IgM  pentamers (5 monomers linked)
SSSSSKKKKKIIIIIPPPPP
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Work to inactivate antigens by: (* most important to body protection)
o Complement fixation (can be innate or active)*
 Described earlier in innate; MAC; used against cellular antigens like bacteria
and wrong RBCs; can bind to antibodies that have attached to the surface of an
antigen; causes lysis of antigen which releases molecules that enhance the
immune response
o Neutralization *
 When antibodies bind to bind to specific sites on bacterial exotoxins (toxic
chemicals secreted by bacteria cells) or viruses to prevent the toxins from
injuring the host’s cells
o Agglutination
 Clumping of foreign cells, possible b/c are multiple antigen-binding sites on
each antibody that can cause large, cross-linked lattices of antigens and
antibodies
o Precipitation
 When cross-linked antibodies and antigens make such a large clump that the
substance is no longer dissolved and forms a solid  easier for phagocytes to
destroy antigens b/c are clumped together and can’t move away from clump
Cellular (Cell-Mediated) Immune Response
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T cells are activated (to make clones) when they bind to a recognized antigen
Can’t bind to free-floating antigens, can only bind to antigens presented on the surface of a
macrophage via double-recognition
o Macrophage eats antigen  processed inside the macrophage  parts of antigen are
displayed on macrophage’s surface “antigen presentation”  T cell recognizes both
self and antigen molecules
o Macrophages also release cytokines  chemicals released by activated T cells,
macrophages, & others immune cells (TABLE 12.3)
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Many type of T cell clones are made when T cells are activated to provide immunity
o Cytotoxic T cells AKA killer T cells
 Kill virus-infected, cancer, and foreign graft cells
 Binds to foreign cells and releases toxic chemicals (perforins & granzymes from
granules)
 Perforins create holes in cell’s plasma membrane
 Granzymes then enter and destroy the proteins in the cell
 Killer T cell then detaches and finds another antigen
o Helper T cells “directors of immune system”
 When activated, circle through immune system & recruit other immune system
cells to help
 Interact w/ B cells that have already attached to antigens causing B cells
to divide and make clones faster & signals for antibody production
 Release cytokine chemicals that help the body destroy antigens by:
o Stimulating the cloning of cytotoxic T cells & B cells
o Attracting other WBC that work by chemotaxis like neutrophils
o Inc. macrophage’s destruction of microorganisms
o Regulatory T cells
 Release chemicals that suppress the activity of both B and T cells
 Necessary when time to wind down and stopping the immune response after
an antigen has been destroyed
 Prevents unnecessary immune activity
o Memory T cells
 “remember” antigen so next time the encounter is stopped faster and attack is
more intense  part of immunological memory
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