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Mechanisms of Disease > Immunology Lecture 1 > Flashcards

Immunology Lecture 1 Flashcards

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1
Q

People with Rh positive blood type have what on their RBC?

A

D antigen

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2
Q

When exposed to the D antigen, which antibody do Rh negative patients make?

A

IgG

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3
Q

If an Rh positive man has a child with a Rh negative woman, when are antibodies produced? Why is this a problem?

A

During delivery, in the next Rh positive pregnancy antibodies will attack fetal blood cells

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4
Q

What are the major antigen targets of rejection?

A

Major histocompatibility complex molecules

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5
Q

What is the name of MHC molecules in humans?

A

human leukocyte antigens

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6
Q

What are the classes of HLA antigens and where are they found?

A

Class I is found on all nucleated cells, class II is on dendritic cells, macrophages, and B cells

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7
Q

How is a donor matched with a recipient? What would the recipient be given to prevent a reaction?

A

The organ donor and recipient are typed based on similar HLA tissue expression. The recipient is given suppressive therapy to inhibit their immune response

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8
Q

What is an autograft?

A

From one part of the body to another

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9
Q

What is an allograft?

A

Between different members of the same species

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10
Q

What is a syngeic graft?

A

Between genetically identical individuals (EX twins)

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11
Q

What is a xenograft?

A

Between members of different species

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12
Q

What are the 3 types of rejection?

A

Antibody-mediated (hyperacute and acute), cell-mediated (acute), chronic rejection (chronic)

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13
Q

What are the symptoms of rejection (3)?

A

General discomfort, uneasiness, or ill feeling; flu-like symptoms (chills, body aches, nausea, cough, shortness of breath); symptoms depending on the transplanted organ (EX: high blood sugar in a pancreas transplant)

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14
Q

What are the characteristics of an hyperacute transplant rejection? What type of reaction is this? When is this often seen?

A

Antibody mediated
Occurs immediately when preformed anti-blood group antigen or anti-HLA antibodies bind to vascular endothelial cells of a graft

Complement is activated, antibodies against HLA antigens are deposited in the tissue. neutrophils, macrophages, and platelets are attracted to the site causing further damage.

Platelet deposition leads to vascular thrombosis. This is seen in ABO blood type incompatibility

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15
Q

What mediates an acute transplant rejection?

A

T cell mediated or antibody-mediated

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16
Q

What are the characteristics of a T cell mediated acute rejection reaction?

A

Occurs within the first week and can last for several weeks.

Antigen presenting cells present donor alloantigens to host T lymphocytes

If APCs are from the donor —> direct pathway to T cell activated
If from the recipient —> indirect pathway T activation

CD8 cells will recognize MHC I molecules, differentiate into mature CTLs, and directly kill graft tissue. CD4 cells will recognize MHC II molecules, differentiate into T helper effector cells, and secrete cytokines to increase vascular permeability, bring immune cells to site, and activate macrophages to cause graft injury

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17
Q

What are the characteristics of antibody-mediated acute reaction?

A

AKA humoral rejection
-B lymphocytes proliferate and then differentiate into plasma cells
-Plasma cells produce donor-specific antibodies (either newly produced or from pre-transplantation exposure)
-Previous exposure causes the rejection but antibodies develop after transplantation
-complement-fixing antibodies are generated and graft vasculature is targeted causing rejection

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18
Q

What are the characteristics of chronic rejection?

A

-Occurs over years due to inadequate immunosuppression
-Residual circulating anti-graft T lymp cells or antibodies compromise graft
-causes fibrosis, vascular injury/impaired blood supply, loss of graft function due to T lymphocyte and macrophage infiltration and cytokine production that stimulates fibroblasts
-eventually leads to endothelial smooth muscle thickening and arterial occlusion

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19
Q

What are the 3 fundamental requirements for development of GVHD?

A

Graft must contain immunologically competent cells, recipient must express antigens that are not present on donor cells, recipient must be immunologically compromised

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20
Q

Why does graft versus host disease occur?

A

Donor T cells react to HLAs on host cells and attack the transplant recipient’s body

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21
Q

What is the timeline of development of graft-versus-host disease

A

Can be acute (months) or chronic (years) but typically occurs within first 100 days

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22
Q

What are the symptoms of graft versus host disease?

A

GI tract- diarrhea, abdominal cramping, nausea, anorexia, possibly GI bleeding
Skin-rash, itching, blisters, and ulcerations. Rash starts on hands and feet and spreads
Liver-jaundice, liver disease

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23
Q

How do you prevent and treat graft rejection?

A

Immunosuppresion prevents and treats rejection by inhibiting T cell activation and effector functions. You can use cytotoxic drugs, immunosuppressive agents, and anti-T cell antibodies.

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24
Q

Why does autoimmunity occur?

A

The immune system fails to differentiate self vs nonself

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25
What is self-tolerance?
The ability of the immune system to differentiate self from non-self
26
What are the 2 processes involved in self-tolerance?
Central tolerance- eliminating auto reactive lymphocytes during maturation in lymphoid tissues, peripheral tolerance- suppression of auto reactive circulating lymphocytes that escaped destruction
27
What mechanisms are responsible for tissue injury in autoimmunity?
Circulating autoantibodies, immune complexes, and auto reactive T lymphocytes
28
What are the main factors that impact the development of autoimmunity?
Susceptibility genes and environmental triggers
29
What sort of mutations are not usually responsible for autoimmunity?
single-gene mutations
30
When susceptibility genes are in combination with environmental factors, what are you at an increased risk for?
Autoimmunity
31
In autoimmunity, the expression of inherited genetic variations depends on certain environmental ___. What are some examples of these?
Triggers: viral infections, chemical substances, or self-antigen from host body tissue that was hidden during development and is now suddenly expressed
32
If disruption of a step during antigen recognition occurs what can happen?
Loss of self-tolerance
33
What are the 4 ways loss of self-tolerance can happen due to disruption of antigen recognition in autoimmunity?
T-cell anergy- an antigen-specific T cell cannot respond to an appropriate stimulus due to reduced function Release of sequestered antigens- hidden self-antigens are reintroduced to the immune system Molecular mimicry- similarities between foreign and self-antigens cause an immune response against auto-antigens Superantigen formation- presence of a family of substances (staphylococcal and streptococcal exotoxins) can activate T lymphocytes leading to fever, shock, and death
34
When immune responses function inappropriately, they can cause ___
Tissue injury and disease
35
What is hypersensitivity?
Abnormal/excessive activated immune response that damages host tissue
36
What are the 2 categories that disorders caused by hypersensitivity reactions can fall into?
Abberant (wrong) immune response and excessive immune response
37
Why might hypersensitivity occur?
Uncontrolled or dysregulated response to foreign antigens or response directed against self antigens resulting in autoimmune disease
38
Are hypersensitivity responses adaptive or innate?
Adaptive
39
How are hypersensitivity reactions categorized?
Based on the principle immunologic mechanism that is responsible for tissue injury and disease
40
What are the 4 categories of hypersensitivity reactions?
Type I-IgE mediated Type II- antibody mediated Type III- complement-mediated Type IV- T cell mediated
41
What do clinical and pathologic features of hypersensitivity depend on?
Mechanism of immune response and location of target antigen
42
Describe Type I hypersensitivity reactions
Mediated by IgE Classic allergic response Antigens that cause immediate hypersensitivity = allergens Person developing symptoms to allergens = atopic High IgE and atopy runs in family but the target organ is variable
43
What is the mechanism that Type III hypersensitivity reactions cause tissue damage?
Type III is immune complex-mediated IgG or IgM antibodies react with soluble antigens that form immune complexes in the bloodstream and are deposited in tissues These reactions can be systemic or localized and the clinical manifestations depend on site of immune complex deposition. The result is inflammation leading to tissue damage
44
Why does damage occur in type IV hypersensitivity reactions?
This is a T cell-mediated disease. Activation of antigen specific Th1 cells result in inflammation mediated by macrophages and tissue damage from cytotoxic T cells
45
What are the target antigens of T-cells in Type IV hypersensitivity reactions?
Innocuous environmental antigens, self antigens as a part of autoimmune processes, or intracellular pathogens that are hard to clear
46
Which antibodies are formed in type II hypersensitivity reactions?
IgG and/or IgM against cells or tissue antigens on host cell tissues
47
What antigens do type II hypersensitivity target?
Red blood cell antigens, solid tissue antigens, receptors on tissues
48
What determines the clinical manifestation of Type II hypersensitivity reactions? What is the consequence of the hypersensitivity?
The tissue that expresses the target antigen, inflammation causes destruction or dysfunction of cells/tissues
49
What is the treatment for hypersensitivity?
Anti-inflammatory drugs, immunosuppression for reactions against self antigens, antigen avoidance and desensitization for immediate hypersensitivity
50
What is immunodeficiency?
Immune system abnormality that results in increased susceptibility to disease that would normally be eradicated by a properly functioning immune response
51
What are the types of immunodeficiency and what do they mean?
Primary-genetic disorders Secondary-acquired during life
52
What causes primary immunodeficiencies?
Defects in lymphocyte development, lymphocyte activation, and effector mechanisms of innate or adaptive immunity
53
What are the warning signs of primary immunodeficiency diseases (10)?
1) frequent ear infections 2) frequent sinus infections 3) prolonged antibiotic therapy 4) little antibiotic effect 5) failure to thrive 6) recurrent abscesses 7) two deep-seated infections 8) persistent thrush or fungus infections 9) need for IV antibiotics to clear infections 10) family history of primary immunodeficiency diseases
54
What is the pathophysiology of primary immunodeficiency?
A genetic abnormality leads to altered protein production that is essential to a fully functioning immune system. Effects depend on the specific gene mutated and can range in severity from mild to life threatening
55
What is the deficiency in severe combined immunodeficiency?
Reduced number of B cells, reduced number of T cells, and reduced serum immunoglobulin
56
What are the primary features of SCID?
Recurrent infections around 6 months of age, severe common viral infections and bacterial infections, prone to opportunistic organisms, failure to thrive, babies usually die within a year
57
What is the genetic basis of B cell deficiency?
Genetic defects in antibody genes or in genes needed for T helper cell development
58
What are the functional defiencies in B-cell deficiency?
Reduced numbers of B cells or skewed B cell production of antibodies
59
What are the primary features of B-cell deficiency?
Pyogenic bacterial infections, enteric bacteria and viral infections
60
What are examples to know of B cell deficiency?
X-linked agammaglobulinemia and selective IgA deficiency
61
What causes and happens in X linked agammaglobulinemia?
Inability to produce B cells or their immunoglobulins. Also called bruton type because gene that codes for bruton tyrosine kinase, which is important for B cell maturation, is mutated
62
What are the causes of selective IgA deficiency?
Possibly genetic, sporadic. Could be caused by lack of breastfeeding at birth or medications/viral infections.
63
What happens in selective IgA deficiency?
Little to no IgA results in recurrent infections. It is also associated with many autoimmune conditions such as RA, Lupus, and Celiac disease
64
What is the genetic basis of T cell deficiency?
Defect in genes needed for T cell development or activation, incomplete development of the thymus
65
What lab findings would be present in T cell deficiency?
Reduced numbers of T cells, possibly decreased serum immunoglobulin
66
What are the primary clinical features of T cell deficiency?
Severe common viral infections and other intracellular microbial infections, virus associated malignancies
67
What is an example of T cell deficiency to know?
DiGeorge syndrome
68
What causes DiGeorge Syndrome?
Absence of a portion of chromosome 22. Can be familial or sporadic
69
What happens in DiGeorge syndrome
Poor development of multiple body systems, underdeveloped thymus leads to low T cell counts and increased susceptibility to infection
70
What are the primary features of a defect in innate immunity?
Severe infection or sepsis, absence of pus
71
What are the functional deficiencies of a complement deficiency?
Decreased levels of specific complement components or disorders that normally would inhibit complement activation on human cells
72
What are the primary features of a complement deficiency?
Increased infections
73
How can a primary immunodeficiency disorder be treated?
Antibiotic therapy, symptomatic care to control infections through periodic injection of intravenous immunoglobulin or subcutaneous immunoglobulin In severe cases, bone marrow transport may be necessary
74
A secondary immunodeficiency is a ___ immunodeficiency
Acquired
75
What can cause a secondary immunodeficiency (5)?
Immunosuppressive agents; malnutrition; aging; medications; diseases such as cancer, chronic infections, or AIDS that directly or indirectly cause immunosuppression
76
What causes AIDS?
Infection with HIV
77
AIDS is characterized by ___ which triggers other abnormalities
Immunosuppression
78
What cells of the immune system does the AIDs virus infect?
CD4 T helper cells, macrophages, dendritic cells
79
How is AIDs currently treated
There is no vaccine or cure but antiretroviral therapy can be effective
80
What is the pathogenesis of HIV infection
HIV binds to a CD4 cell and enters. The virus uses reverse transcriptase enzyme to convert RNA to DNA for replication and integrates its DNA with CD4 DNA. HIV viral DNA forms mRNA. RRNA makes poly protein from mRNA instructions. Cleavage occurs to create multiple HIV proteins for viral replication. The virus leaves CD4 cell to spread
81
During the acute/early infection phase of HIV, what clinical features would you see?
Fever, headache, sore throat, generalized lymphadenopathy, and rashes Symptoms develop 3-6 weeks after infection
82
What is the pathophysiology of an acute HIV infection?
Spike of virus in blood and small reduction in CD4 T cells
83
What happens during the clinical latency phase of HIV?
Patients are asymptomatic or suffer from minor infections. This phase may last for many years. CD4 T cell count declines. Macrophages and follicular dendritic cells act as reservoirs for HIV.
84
What would you see in AIDS?
Opportunistic infections, wasting syndrome, and dementia as CD4 T cell count falls below 200 cells/microliter
85
What are the risk factors to be concerned about with AIDS?
Sexual activity, exposure to blood
86
What are early signs and symptoms of infection with HIV?
Flu like symptoms
87
What treatments are used for HIV?
Highly active antiretroviral therapy that suppresses viral entry and replication and delay disease progression. Drugs in combination that reduce the development of drug resistance

Mechanisms of Disease (6 decks)

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