immunity Flashcards
Adaptive immunity ____ with prior infections/antigens?
remembers antigen
humoral adaptive vs cell mediated memory?
humoral=b cells –>mostly bacterial and viruses (outside invaders)
cell mediated = t cell –>Tc cells =cytotoxic –>kills viruses and cancers (infected cells)
innate vs adaptive defenses; memory vs speed (1st exposure and 2nd exposure)
adaptive: slow 1st exposure, but remembers and Faster than innate on 2nd exposure. adaptive includes humoral and cell mediated.
innate: fast 1st exposure. slower than adapt in 2nd exposure.
innate vs adaptive immunity, which cells in each?
adapt: T & B
innate: antimicrobial proteins/phagocyctes, compliment/NK cells.
is innate immunity a process?
no, not when compared to adaptive.
does innate and adaptive immunity talk?
they can yes.
adaptive immunity and inflammation and non self substances
adapt and inflam work work together, recognize non self substances aka” antigens” (pathogens, allergens, transplants)
lymphocytes vs antibodies immunoglobulins, adaptive immunity end products?
cell mediated: lymphocytes / t cells
humoral immunity: B cells, immunoglobulins (IG)
how b cells and t cells differ?
in response to antigens, B cells secrete antibodies where as T cells kill antigens directly. Both B and T remember.
humoral and cellular immunity do this to provide immunity and memory, and it has this effect on 2nd antigen exposure
work together, more rapid and efficient response w/2nd exposure
clonal diversity vs selection
SELECTION: DIFFERENTIATION of B->antibody producing / plasma cells & T cells->effector cells. think “caught something” and going after it. in spleen (t cell) and lyph (b cell). this is where b cells do their thing as plasma cell producing stuff, and t cells do their thing becoming t effector cells, so that they can go after this infection.
DIVERSITY (clonal): each T and B cell recognize one antigen and sum of them protect against many. IN thymus (t cell), Bone marrow (b cell)
what are the primary and secondary lymphoid organs where clonal diversity takes place?
primary/central: thymus, fetal liver, bone marrow (immature)
secondary/peripheral: spleen lyph, tonsils, adenoids
what initiates clonal selection?
foreign antigen
hypersensitivity, is this a true system?
it is an artificial system. because they are not mutually exclusive.
Once sensitized reactions can be _____ or ____
Immediate hypersensitivity reactions-after a single exposure; min-hrs (anaphylaxis)
Delayed hypersensitivity reactions-may require multiple exposure that occur over years; several hours-days
The most rapid and severe immediate hypersensitivity reaction is ______
anaphylaxis
anaphalaxis
Occurs within minutes
Systemic (generalized): itching, erythema, headaches, vomiting, abdominal cramps, diarrhea, and breathing difficulties
Severe cases: contraction of bronchial smooth muscle, laryngeal edema, and vascular collapse may result in respiratory distress, decreased blood pressure, shock, and death
Allergens induce ___by which Ig?
Type I hypersensitivity, generally against environemnt
mediated by IgE
prostaglandans can activate ___ receptors
pain
leukotrienes are important in treating __
asthma.
first exposure is always
sensitivation
dendritic cells are ___
antigen processing cell, makes antibodies against it
Sensitization
. The IgE coats the surface of the mast cell by binding with IgE-specific Fc receptors on the mast cell’s plasma membrane (sensitization).
IgE – allergies
allergic reaction, leaky vessels,
histamine binds to what receptors?
H1 receptors, any tissue with this can respond. Brochiosmooth muscle to constrict/wheezing, increase vasc perm (endo leaky), blood flow increase and now edame and swelling.
h2 receptors have what effect
N/V in anafalax
initial vs early
initial within 5-30 minutes, late phase 2-8hrs later (intense infiltration, tissue destruction/endothelial)
clinical manifestations of histamine effects ___ cells, which ones have a lot?
mast cells. GI, Resp, Skin.
clinical signs of type i hypersensitivity
vasodialate, heart
signs of anaphylactic rxn with a kid with bee sking. can you die? what kind of rxn is this?
eyes and lips swell, systemic systems (flushing, sweating, dizzy, and GI, resp, vascular) aka from dropped BP can go to shock.yes. type 1
type II hypersensitivity
a specific cell or tissue being the target, are called tissue-specific antigens.
can also occur in autoimmune disorder.
CN allergy
hemolytic anemia
opsonins from __ system and which C?
tag (c3b) from compliment system.
Define **allergy, hypersensitivity, autoimmunity and alloimmunity
**Allergy: Is an exaggerated response against an environmental antigen.
Autoimmunity: Is a misdirected response against the host’s own cells.
Alloimmunity: Is directed against beneficial foreign tissues (e.g., transfusions, transplants)
Immunodeficiency: Immunity is insufficient to protect the host.
All responses can be serious or life threatening.
Target Cells Destroyed by Phagocytosis which type?
Antibody causes cell destruction through phagocytosis by macrophages. II
Target Cells Destroyed by Neutrophil Granules which type?
Antibody and complement attract neutrophils . The components of neutrophil granules, as well as the several toxic oxygen products produced by these cells, will damage the tissue. II
Target Cells Destroyed by NK Cells, which type?
Antibody-dependent cell-mediated cytotoxicity (ADCC)
Fc receptors on the NK cells, which release toxic substances that destroy the target cell. II
Target Cells Destroyed by Cell Malfunction, which type?
Causes target cell to malfunction (not destroyed), II
Type III Hypersensitivity is _____ mediated.
Immune (antigen-antibody) complex mediated.
Complexes are formed in the circulation and deposited later in vessel walls or extravascular tissues
what is the damage due to in type III hypersensitivity
c5a (lysozomes),
what is the damage due to in type III hypersensitivity
c5a (lysozomes), and C3b that further causes inflammation.
clearance in III
larger by macrophages, small cleared by kidney (renal), intermediate –>deposits in tissues.
is an immune complex that is but it gets stuck in the tissues .
what is the damage due to in type III hypersensitivity
c5a (lysozomes), and C3b that further causes inflammation. of complement system.
Damage results from complement activation (C3b) and c5a
clearance in hypsersens III
larger by macrophages, small cleared by kidney (renal), intermediate –>deposits in tissues.
is an immune complex that is but it gets stuck in the tissues .
Immune Complex Disease- Serum Sickness is caused by repeated ___ and type ___
iv, type III, Affected tissues are blood vessels, joints, and kidney.
Symptoms: fever, enlarged lymph nodes, rash, and pain at sites of inflammation
Immune Complex Disease-Serum Sickness, one form is One form with Cryoglobulins is what does what?
Raynaud phenomenon, Blocks circulation and causes localized pallor or numbness. is a temporaryCertain immune complexes precipitate at temperatures below normal body temperature, particularly in the tips of the fingers, toes, and nose, and are called cryoglobulins.
Arthus Reaction is a ___ that causes
Immune Complex Disease-Serum Sickness.
the prototypic example of a localized immune complex–mediated inflammatory response. It is caused by repeated local exposure to an antigen that reacts with preformed antibody and forms immune complexes in the walls of the local blood vessels. Symptoms of an Arthus reaction begin within 1 hour of exposure and peak 6 to 12 hours later. The lesions are characterized by a typical inflammatory reaction, with increased vascular permeability, an accumulation of neutrophils, edema, hemorrhage, clotting, and tissue damage.
Allergens that induce Type II and Type III hypersensitivity, if allergic to milk it could be?
metabalyte of penicillin.
Certain individuals are genetically predisposed to develop allergies, particularly type I allergies, and are called
atopic
type 4 hypersensitivity is ___ mediated
cell mediated.
. destruction by cytotoxic t cells.Helper T (Th) 1 and Th 17 cells produce cytokines
type 4 hypersensitivity examples ___
Acute graft rejection
type 4
antibodies that destroy antibodies. Development of Allergic Contact Dermatitis, a Delayed Hypersensitivity Reaction. A, Shown here is the development of allergy to catechols from poison ivy. No dermatitis results from the primary contact because the antigens (catechols) are sensitizing the immune response and producing memory T cells.
Allergic Contact Dermatitis
type 4, first time no worries, second time issue.
type 4 hypersensitivity examples
to a plant (poison oak), to nickel (metals), checmicals, antibiotics.
Type I vs Type IV Skin Reactions
can have both. compare and contrast. I (IgE), Iv (T-cells) both cause skin rxn, distribution of skin leason may tell you. atopic (widely dist), delayed type (local)
Type I vs Type IV Skin Reactions
can have both. compare and contrast. I (IgE), Iv (T-cells) both cause skin rxn, distribution of skin leason may tell you. atopic (widely dist), delayed type (local)
