BLD unit 2 Flashcards
(173 cards)
1
Q
what are the characteristics of human adaptive immunity
A
memory, antibody production, discrimination between self vs non-self
2
Q
describe self vs non-self
A
antigens presents on the surface of cells show the immune cells if they are the host cells of if they are “bad” cells.
3
Q
what is the portion that is recognized for self vs non-self
A
the epitope of the antigen
4
Q
what are the two portions of adaptive immunity
A
humoral and cell mediated
5
Q
what are the two types of lymphoid tissue
A
primary and secondary
6
Q
where do primary lymphoid tissue cells come from
A
Thymus and Bone marrow, cells differentiate and mature into lymphocytes here
7
Q
where do secondary lymphoid tissue cells come from
A
lymph nodes, spleen, MALT: where adaptive immune responses develop
8
Q
what does MALT stand for
A
mucosa associated lymph tissue
9
Q
list some innate components
A
epithelial barrier, pH of certain regions within body, phagocytes (neutrophils and macrophages), NK cells,
10
Q
what type of cell are NK cells?
A
lymphocytes
11
Q
what do NK cells do?
A
recognize the loss of “MHC I” (self) molecules on cells that are malignant or virus-infected, also recognize Stress-Induced Ligands
12
Q
what type of immunity are NK cells a part of?
A
innate, because they don’t recognize a very specific antigen on the surface of problem cells.
13
Q
what is the mechanism for NK cells
A
release perforin and granzyme that both lead to apoptosis, or Engage Death Receptors
14
Q
what are the example of cell surface proteins that help us identify variable lymphocytes
A
CD#
15
Q
where are T cells derived from
A
thymus
16
Q
where are T cells found
A
blood, spleen, around arterioles, lymph node
17
Q
what do T cells NOT do
A
they do NOT detect free antigens… they have to be PRESENTED to the T cell by MHC molecules (B cells, macrophages, and dendritic cells)
18
Q
what cells are the effector cells that help the B cells produce antibodies
A
T cells
19
Q
describe characteristics of TCR’s
A
membrane bound, two peptide chains, variability is made my rearrangements of gene segments (V,D,J)
20
Q
what is the name for MHC but for humans
A
HLA (human leukocyte antigens)
21
Q
what type of T cell is involved with cell mediated immunity and what surface proteins are specific to them?
A
cytotoxic T cells (Tc), are CD8+
22
Q
what are Tc cells involved in?
A
direct killing of cells that present non-self antigen, also produce a LOT of cytokines
23
Q
what type of immunity are T helper cells involved with?
A
humoral immunity (stimulate B cells to produce antibodies)
24
Q
describe characteristics of MHC I
A
(mostly endogenous) present on all nucleated cells, present antigens (self or non-self) to Tc cells, have a heavy alpha chain and beta 2- microglobulin chain
25
describe characteristics of MHC II
(mostly exogenous) present on professional APC's, consumes antigen and processes it to present on MHCII on APC, two peptide chains that are more equal in size, signal recognized by CD4+ helper T cells
26
where are B cells derived
Bone marrow
27
what type of immunity are B cells involved in
humoral immunity (produce antibodies once they are plasma cells)
28
where are B cells found
bone marrow, spleen, circulation, MALT, lymph node follicles
29
what do B cells recognize
free antigen, do not require MHC presentation
30
how are IgM's related to B cells
functions as the antigen-binding component of the BCR.
31
describe class switching within B cells
Once activated, the B cell can undergo class switching from IgM to other antibody forms like IgG, IgA, or IgE, depending on cytokine signals from helper T cells.
32
how many classes of AB are there?
5
33
what are the types of light chains?
kappa an lambda
34
what are the main functions of antibodies?
agglutinate and lyse bacteria, opsonize bacteria, initiate complement, neutralization of toxins, assist NK cells
35
IgG
70-80% of Ig, monomeric, neutralizes toxins, opsonization
36
what is unique about IgG
is the only class that crosses the placenta
37
IgA
dimer (J chain connection), within: mucosa, tears, sweat, bile, and breast milk, stops bacteria and viruses from entering the epithelium at the start
38
IgM (biggest)
largest Ig, pentamer or monomer, joined at Fc fragments by J chain, 10 binding sites (2 for each Ig)
39
what is unique about IgM
first after immunization, first class
40
IgE
Fc fragment binds to receptors on MAST cells (release histamines), antigen binding results in release of granules (histamines and leukotrienes) and calls eosinophils, PARASITIC infections
41
what is unique about IgE
involved in hypersensitivity
42
IgD
present on some B cells, helps with antigen recognition (with IgM)
43
what is unique about IgD
helps "arm" basophils and MAST cells in mucosa to help with immune surveillance... binds to cells in mucosa
44
what is the function of APCs
to capture and display the antigen in MHC II molecules
45
what are the 3 types of APCs
dendritic cells, macrophages, B cells
46
what is unique about dendritic cells
found in the T cell zones in lymphoid tissue
47
what is unique about B cells as APCs
first bind to antigen with BCR, then take it in and process Ag, then present Ag via MHC II to T helper cells
48
what is the IL-2 cytokine do that is important with lymphocyte
lymphocyte clonal expansion
49
through what mechanism do B cells present antigens?
MHC II
50
through what mechanism do B cells detect antigens
BCR
51
describe somatic recombination
provide diversity of BCR and TCR antigen binding sites
52
B and T cells develop from what type of cell and where do they produce these cells
lymphoid progenitor (LP) cell, produce B and T cells in the bone marrow
53
after LP gives rise to TP (T cell progenitor) what happens to it
TP leaves the bone marrow and heads to the thymus
54
what are the segments of the heavy chain
V D J C
55
what are the segments of the light chain
V J C
56
within B cell recombination which chain is rearranged first?
heavy chain
57
describe somatic recombination
VDJ gene rearrangement products are transcribed and translated into protein that will become the heavy chains of AB, same with light chain (VJ)
58
cell mediated immunity is done by what type of cell
cytotoxic T cell (Tc)
59
MHC I presents antigen to what kind of T cell
Tc cell (CD8+)
60
if CD8+ cell interacts with Ag on MHC I what will happen next
CD8+ stimulates apoptosis in the infected cell
61
CD8+ also do what
produce and release cytokines
62
T cell proliferation requires what cytokine
IL-2
63
what is step 1 of humoral immunity
B cell recognizes antigen with BCR
64
what are the two types of B cell activation
T independent and dependent
65
B cell activation that is T independent creates what type of B cell
antibodies without memory
66
T independent produces what AB
IgM
67
why is B cell activation less likely to occur without T cells
most antigens are not able to activate B cells, need T helper cells
68
explain T dependent B cell activation
once antigen is recognized, ingested, presented on MHC II, CD4+ T helper cells recognize the presented antigen (linked recognition)
69
what cytokines stimulate differentiation into antibody-producing cells
IL-4, IL-6, IL-10, and IFN-gamma
70
what type of B cells make antibodies
plasma cells
71
antibodies that are made from B cells have the same specificity as
original BCR
72
class (isotype) switching
the constant Fc region of the heavy chain is changed to another type, antigen specificity remains the same
73
what is an example of isotype switching
IgM to other Ig
74
which type of immunity is faster
innate is faster than adaptive
75
which is faster primary immune response or secondary
secondary is quicker because memory helps fight off bacteria faster
76
what is primary immune response
the first response to a infection and seeing an infection for the FIRST time
77
what is secondary immune response
building memory to the infection that has previously been seen and reacted to by the immune system
78
what are the 4 main types of Immune disorders
hypersensitivity, autoimmunity, immune deficiency, and neoplastic changes in immune cells
79
define hypersensitivity
an excessive response that causes damage to organism
80
what are the 4 types of hypersensitive reactions
type I, type II, type III, Type IV (ACID)
81
what are the names for type I
immediate, allergy, reagin-activated
82
what are the main molecules within Type I sensitivity
TH2 cells, IgE, and mast cells
83
describe the first exposure to the antigen/allergen in Type I hypersensitivity
TH2 cells are activated and influence class switching to IgE production, IgE binds to mast cells with Fc fragment, this sensitizes mast cell with multiple IgE bound.
84
describe second exposure to allergen in Type I hypersensitivity
antigen binds to IgE bound to mast cell, causing mast cell to degranulate and release histamines which causes vasodilation and increase vascular permeability
85
in Type I hypersensitivity Mast cells produce what mediators
histamine, prostaglandins, proteases, leukotrienes, cytokines
86
what is a common result of Type I
anaphlaxis
87
what is another name for Type II hypersensitivity
cytotoxic hypersensitivity or antibody mediated
88
describe type II hypersensitivity
antibodies bind to self-epitope causing phagocytosis, complement activation, and antibody dependent dysfunction
89
what are the outcomes of type II hypersensitivity
immune hemolysis, graves disease (hyperthyroidism), drug-induced
90
another name for Type III hypersensitivity
immune-complex mediated
91
what is the main problem in type III hypersensitivity
antigen/antibody complexes (size of them), these complexes get deposited into the tissue (causes inflamation)
92
what does type III stimulate
complement activation, vasoactive amines, platelet aggregation
93
what are the outcomes of Type III
vascular smooth muscle damage (necrosis)
94
what are example of Type III
glomerulonephritis, arthritis, serum sickness
95
what is another name for Type IV hypersensitivity
cell-mediated or delayed
96
what is a unique feature of Type IV
no antibodies involved
97
what cells do the damage in type IV
sensory T cells as they have an over response to an antigen
98
what is an example of Type IV
reaction in TB test, tissue organ rejection, granulomatous inflammation, contact dermatitis
99
describe mechanism of Type IV (delayed)
happens 12-48 hrs after exposure, T effector cells secrete cytokines, prolonged response becomes granulomatous inflammaiton
100
describe Type IV (cytotoxic lymphocytes)
kills cells showing the antigen, rejection of transplants
101
define tolerance
lack of response to antigen
102
define self tolerance
normal lack of response to self antigen
103
how do we develop self tolerance?
with central tolerance, peripheral tolerance, seclusion
104
define central tolerance
(in bone marrow and thymus) self reactive T and B cells are deleted early on in development, using apoptosis
105
define peripheral tolerance
(lymph nodes, spleen) self reactive T cells that escape the thymus (central tolerance) can also be stopped by Functionally inactivating self-reactive cells
106
define seclusion
tissues exclude immune cells all together, self-reaction is not a problem
(lens of the eye)
107
define autoimmune damage
damage depends on the immune target, often due to autoantibodies, can be organ specific
108
what are the 4 mechanisms of developing autoimmunity
1) previously secluded tissue proteins are exposed 2) alteration of tissue antigens 3)exposure to 'shared' determinants 4) impaired T cell regulation
109
what is the term for genetic immune disorders
genetic disposition
110
what are the 3 autoimmune disease examples
SLE, Hashimotos, RA
111
describe SLE
BUTTERFLY RASH autoantibodies are ANA (attacks all cells with nucleus), immune complex deposition causes organ damage (skin and joints)
112
SLE is what kind of autoimmunity
genetic predisposition (HLA DR2, DR3)
113
death from SLE is most often from
renal failure, heart problems, or infections
114
describe hashimotos thyroiditis
thyroid, autoantibodies attack thyroid tissue, (Tc cell mediated)
115
goiter is caused from what
hyperplasia
116
symptoms of hashimotos
enlarged thyroid, hypothyroidism, usually middle-aged females
117
describe Rheumatoid arthritis
mainly joint disease, immune complex deposition and damage from cytokines,
118
define immune deficiency
inadequate response to antigen
119
what are the two specific types of immunodeficiency
afferent (antigen presentation and recognition), Efferent (T cell activation and antibody production)
120
describe examples of non specific immune deficiencies
complement deficiency unable to kill bacterial cells, phagocytosis problems (cannot take in problems)
121
describe primary deficiency
congenital and are genetic
122
describe secondary deficiency
acquired, develop from another problem previously
123
list 3 primary deficiencies
SCID, DiGeorge syndrome, Bruton disease
124
describe main components of SCID
congenital, affects both T and B cell function, thymus is hypoplastic (low tissue), other tissues are atrophic, often seen in INFANTS
125
how is the immune system with SCID
no antibodies or cell mediated response (Tc)
126
what are the 2 genetic defects of SCID
1) ADA deficiency (lack of enzyme) 2) common gamma chain defect (defective receptors for cytokines = no T and B cell proliferation)
127
what is the Tx for SCID
bone marrow transplant
128
describe DiGeorge syndrome
lack of thymus development, genetic defect (deletion of C22), prone to viral and intracellular bacterial infections,
129
describe Brutons disease
X-linked agammaglobulinemia = no antibodies, pre-B cells fail to mature and get into blood, results in repeated infections by bacteria
130
what are some causes of secondary immune deficiencies
age, malnutrition, neoplasia of immune system, infection
131
describe AIDS
viral infection of HIV, depletion of CD4+ lymphocytes (TH cells) = no antibodies
132
how is AIDS spread
blood or bodily fluids that contain virus
133
what are the two main targets of AIDS
immune system and CNS
134
immunodeficiency caused by AIDS effects include
CD4+ T cell loss, defective DC and macrophage function, damage to lymphoid tissue
135
what part of AIDS makes it hard to produce a vaccine
has a high viral mutation rate, constantly changing antigens for immune system to target
136
how do CD4+ T cells die from AIDS
loss of precursor or infection in them, chronic activation by HIV antigen apoptosis, direct cell lysis by virus, killing by cell mediated immunity (CTLs)
137
define amyloidosis
diseases characterized by the abnormal accumulation of Beta-pleated sheets creating sticky fibrils
138
what is the unifying feature of amyloidosis
fibrils made of beta-pleated sheets
139
what does amyloidosis look like macroscopically in organs?
larger, firmer, paler
140
describe immune origin amyloidosis
(primary or secondary) over expression of plasma cells that produce abnormal antibodies (light chain) that accumulate and form fibrils, seen in myeloma
141
symptoms of immune origin amyloidosis
carpal tunnel syndrome, macroglossia, neuropathy
142
describe reactive systemic amyloidosis
secondary, due to chronic inflammation/infection, deposits of serum amyloid A (SAA)
143
what does reactive systemic amyloidosis signal for
upregulation of IL-2, TNF-alpha, and IL-6
144
what are the symptoms of reactive systemic amyloidosis
primarily affects the kidneys, liver, spleen, and adrenals, most commonly renal failure
145
describe hemodialysis-associated amyloidosis
secondary, occurs in patients that have been on long term hemodialysis, accumulation of deposits of Abeta2M fibrils
146
what is the protein precursor for hemodialysis-assciated amyloidosis
beta2 microglobulin, unable to be cleared from the kidney
147
what is the common outcome of hemodialysis-associated amyloidosis
carpal tunnel syndrome
148
describe hereditary systemic amyloidosis
primary, genetically inherited disorder caused by mutations in transthyretin
149
what is the source of hereditary systemic amyloidosis
deposits in plasma
150
what are the two types of hereditary systemic amyloidosis
neuropathic and cardiopathic
151
during transplantation what molecule do they match
HLA (human leukocyte antigen)
152
describe autograft
transferring graft from different sites on same organism
153
describe iso graft
two identical organisms (twins)
154
describe allograft
between 2 closely related organisms
155
describe xenograft
use another organism (ex: pig)
156
what are the 2 components of HLA matching
HLA-1and HLA-2
157
characteristics of HLA-1
(genes A, B, C) on all nucleated cells, has a longer chain and a shorter chain
158
characteristics of HLA-2
(genes D,P, DQ, DR) only on APCs equal chain lengths
159
how do you inherit HLA gene
one allele of each gene from each parent
160
what are the different ways of typing HLA genes
serological, molecular, cellular testing
161
describe serological testing
looking for AB/AG interactions between donor and recipient
162
describe molecular testing
tests for differences in the DNA of HLA genes, PCR and probes detect different alleles
163
describe cellular testing
mix lymphocytes from donor and recipient, look for evidence of positive reaction (proliferation, cell-mediated toxicity, cytokine production)
164
describe testing for solid organs
ABO (blood) compatible, HLA matched (kidney 6 antigen), HLA-A,B, DR
165
describe matching for bone marrow
ABO (blood), 10 antigen match (HLA- A, B, C, DR, DQ
166
describe hyper acute transplant rejection
minutes to hours, preformed antibodies in hosts plasma bind to graft endothelium
167
what is the effects of hyper acute transplant rejection
fibrinoid necrosis, ischemia, thrombosis
168
describe acute transplant rejection
early (7-10 days), late (11 days- 6 weeks)
169
what type of immune response in acute rejection
Tc or antibody mediated
170
describe acute cellular rejection
within first months, renal problems, lots of CD4+ and CD8+ cells in organ
171
describe acute humoral rejection
antibody mediated, recipient attacks donor, necrosis, neutrophils, complement, antibody, fibrin, thrombosis
172
describe chronic transplant rejection
months to years post transplant, antibodies bind to HLA on endothelium (vasculature)
173
describe graft vs host disease
mainly bone marrow transplants, donor attacks recipient
