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Flashcards in Chapter 19 Deck (31)


an ABNORMAL antigenic response results from a prior exposure to a foreign substance antigen called an allergen


hypersensitivity: type 1 - anaphylactic

- signs show within 30 minutes. IgE binds to mast cells or basophils and causes degraulation of mast cells or basophil and release of reactive substances such as histamines


anaphylactic: localized

Symptoms: hives, hay fever, asthma--from inhaled or ingested allergens like food or pollen


anaphylactic: systemic

anaphylactic shock, released mediators cause enlargement of blood vessels and a sudden extreme drop of BP (shock), usually from drug injections, insect stings



achieved by repeated injects of the antigen, which leads to the formation of blocking IgG antibodies



Are released chemicals (histamines) which cause the observed allergic reactions



type of mediator, affect smooth muscles of the respiratory system and increase mucus secretion


hypersensitivity: type 2 - cytotoxic

- signs show between 5-12 hours. Antigen causes formation of IgM and IgG antibodies that bind to target cell; when combined with action of complement, it destroys target cell. EX: transfusion reactions; Rh incompatibility (hemolytic disease of the newborn)


hemolytic disease of the newborn

When dad is Rh+ and mom is Rh-, there is a 50% chance the child will be Rh+.

If the child is Rh+, the mother can become sensitized to this antigen during birth when placental membranes tear and fetal Rh+ RBCs enter maternal circulation, causing mother's body to produce anti-Rh antibodies of the IgG type.

If the fetus in a subsequent pregnancy is Rh+, mothers anti-Rh antibodies will cross placenta and destroy fetal RBCs.



HDNB is prevented today by passive immunization of the Rh- mother at the time of delivery of any Rh+ infant with anti-Rh antibodies. These anti-Rh antibodies combine with any fetal Rh+ RBCs that have entered mother's circulation, so it is less likely she'll become sensitized to the Rh antigen.


ABO blood group system

4 principle types of blood: A, B, AB, O.


hypersensitivity: type 3 - Immune complex reactions

- occurs within 3-8 hours; antibodies and antigens form complexes that cause damaging inflammation. EX: glomerulonephritis - inflammation damage to kidney glomeruli


hypersensitivity: type 4 - Delayed cell-mediated, or delayed hypersensitivity

: occurs between 24-48 hours. Antigens activate Tc that kill target cells. EX: rejection of transplanted tissues, contact dermatitis (poison ivy), chronic diseases (tuberculosis)


allergic contact dermatitis

usually caused by haptens that combine with protiens (amino acid lysine) in the skin of some peope to produce an immune response, such as reactions to poison ivy, cosmetics, metals in jewelry, latex,


autoimmune disease

loss of self-tolerance, immune system reacts to self-antigens and causes damage to one's own organs


cytotoxic immune reactions

Involve antibody reactions to cell-surface antigens. EX: Graves' disease, myasthenia gravis


immune complex autoimmune reactions

systemic lupus erythematosus, rheumatoid arthritis


cell-mediated autoimmune reactions

MS, insulin-dependent diabetes mellitus, psoriasis



one's own tissue is grafted to another part of the body



transplantation between identical twins



transplantation between people that are not identical twins


xenograft (xenotransplant)

grafts from animals


HIV infection

retrovirus, has 2 identical strands of RNA, enzyme reverse transcriptase, and an envelope of phospholipid. Envelope has glycoprotein spikes (gp120)


T cells

an immune system cell that plays a central role in cell-mediated immunity


infectivity of HIV

attachment to the target cell depends on the glycoprotein spike (gp120) combining with the CD4+ receptor.

Gp41 participates in fusion of the HIV with the cell. Following fusion with the cell, an entry pore is created.

After entry, the viral envelope remains behind and the HIV uncoats, releasing the RNA core for directing synthesis of the new viruses.

in the host cell, viral RNA is released and transcribed into DNA by the enzyme reverse transcriptase.

This viral DNA then becomes integrated into the chromosomal DNA of the host cell. can either become active or latent.


latent infection

viral dna is integrated into cellular DNA and forms a provirus that can later be activated to produce infective viruses.

A subsetof HIV-infected cells, instead of being killed, become long-lived memory T cells in which the resevoir of latent HIV can persist for decades.

This ability to become a provirus / latent virus shelters it from the immune system


active infection

provirus is activated, allowing it to control the synthesis of new viruses, which bud from host cell.

Final assembly takes place at the cell membrane, taking up viral envelope proteins as the virus buds from the cell.


cell-cell fusion

another way for HIV to evade immune system, by which the virus moves from an infected cell to an adjacent uninfected cell.


transmission of HIV

transmitted by sexual contact, breast milk, contaminated needles, transplacental infection, artificial insemination, and blood transfusion.


CXCR4 and CCR5

best known chemokine coreceptors that are required for HIV to be infective.



virus evades immune defenses by undergoing rapid antigenic changes.

Retroviruses w/ the reverse transcriptase enzyme step, have a high mutation rate compared to DNA viruses.

They lack proofreading also.

As a result, a mutation is probably introduced at every position in the HIV genome many times a day in an inefected person.

This may amount to the accumulation of 1 million variants of the virus in an asymptomatic person and 100 million variants during the final stages of the infection.