Hypersensitivity Rxns Flashcards
(91 cards)
1
Q
What are the two main types of lymphocytes involved in immune reactions?
A
T cells and B cells.
2
Q
Where are MHC class I molecules present?
A
on all nucleated cells.
3
Q
What types of cells express MHC class II molecules?
A
MHC class II molecules are present on specialized cells known as antigen presenting cells (APCs), including macrophages, dendritic cells, and B cells.
4
Q
Define cellular immunity.
A
Cellular immunity involves the activation of T cells to recognize and destroy infected or abnormal cells.
5
Q
What is humoral immunity based on?
A
Humoral immunity is based on the interaction between antigens and antibodies, typically involving B cells producing antibodies against specific antigens.
6
Q
What type of immune response involves the production of antibodies by B cells?
A
Humoral immune response.
7
Q
What cells are responsible for recognizing antigens and producing antibodies?
A
B cells.
8
Q
Which cells differentiate into plasma cells during the humoral immune response?
A
Activated B cells.
9
Q
What do plasma cells produce and release during the humoral immune response?
A
Antiobodies
10
Q
What type of immunity is provided by memory B cells?
A
Long term immunity
11
Q
What type of immune response involves the activation of T cells to directly destroy infected cells?
A
Cell-mediated immune response.
12
Q
What cells present antigens to T cells during the cell-mediated immune response?
A
Antigen-presenting cells (APCs).
13
Q
Which type of T cells directly kill infected or abnormal cells?
A
Cytotoxic T cells.
14
Q
What is the role of helper T cells in the immune response?
A
Helper T cells assist in coordinating the immune response by activating other immune cells and promoting antibody production.
15
Q
What type of immunity is provided by memory T cells?
A
Long-term immunity and a faster response upon subsequent encounters with the same antigen.
16
Q
What characterizes Type I hypersensitivity reactions?
A
Immediate/anaphylactic
17
Q
Which type of hypersensitivity reaction involves antibody-mediated cytotoxicity?
A
Type II hypersensitivity reactions.
18
Q
What is the primary mechanism of Type II hypersensitivity reactions?
A
Antibody-mediated cytotoxicity.
19
Q
Which type of hypersensitivity reaction is immune complex mediated?
A
Type III hypersensitivity reactions.
20
Q
What are the immune complexes composed of in Type III hypersensitivity reactions?
A
Antigen-antibody complexes.
21
Q
What type of immunity is involved in Type IV hypersensitivity reactions?
A
Cell-mediated immunity.
22
Q
Describe the time frame of reaction onset in Type I hypersensitivity reactions.
A
Immediate
23
Q
Which hypersensitivity reaction involves T cells rather than antibodies?
A
Type IV hypersensitivity reactions.
24
Q
What characterizes Type I hypersensitivity reactions?
A
Rapid and intense immunologic reaction.
25
When does a Type I hypersensitivity reaction typically occur after the antigen comes in contact with the antibody?
Within minutes
26
What cells are involved in Type I hypersensitivity reactions, having the antibody bound to them?
Mast cells or basophils (antigen-presenting cells).
27
Which antibody is involved in Type I hypersensitivity reactions?
IgE
28
In Type I hypersensitivity reactions, when does the reaction occur in individuals?
Occurs in previously sensitized individuals to the antigen
29
What are the possible manifestations of local anaphylaxis or reaction?
Depends upon the portal of entry of the allergen, which can include localized cutaneous swellings (skin allergy), nasal and conjunctival discharge (allergic rhinitis, conjunctivitis, hay fever, bronchial asthma), and allergic gastroenteritis (food allergy).
30
Describe the manifestations of systemic anaphylaxis or reaction.
The manifestations range from nausea and vomiting to abdominal cramps, diarrhea, laryngeal obstruction, and can progress to a state of shock, which could be fatal.
31
Name examples of inhaled allergens.
Plant pollen, mold spores, animal dander, dust mite droppings.
32
What are examples of injected allergens?
Insect venom (e.g., bee sting), vaccines, drugs (therapeutic proteins).
33
Provide examples of ingested allergens.
Peanuts, seafood, orally administered drugs (e.g., antibiotics).
34
What are examples of allergens that can be encountered through contact?
Plant leaves, soaps, lotions, metals (e.g., gold, platinum), personal items (e.g., rubber gloves, watches, earrings, rings).
35
What characterizes Type II hypersensitivity reactions?
Antibodies are formed against antigens present on the surface of cells or connective tissue.
36
How do antibodies in Type II reactions bind to cells?
They bind to normal (self) or altered cell-surface (non-self) antigens.
37
What antibody is typically involved in Type II hypersensitivity reactions?
IgM or IgG.
38
Name three mechanisms of cytotoxicity in Type II reactions.
1. Complement-mediated cytotoxicity.
2. Antibody-dependent cell-mediated cytotoxicity (ADCC).
3. Antibody-mediated cellular dysfunction.
39
Describe the process of complement-mediated cytotoxicity in Type II reactions.
Antigen-antibody complexes activate the complement system, leading to the formation of the "membrane attack complex" (MAC), which causes direct cell lysis or opsonization.
40
Provide examples of conditions involving complement-mediated cytotoxicity.
Transfusion reactions, autoimmune hemolytic anemia, erythroblastosis fetalis.
41
Transfusion reactions
Incompatible red blood cells or serum is transfused
42
Erythroblastosis fetalis
Mother is Rh negative with a Rh positive baby
Maternal Rhesus antibodies crosses the placenta and attaches to baby’s red blood cells – causes lysis of red cells (Rhesus incompatibility)
42
Autoimmune haemolytic anemia
Antibody produced against own red blood cells – results in destruction of red cells
43
What occurs in antibody-dependent cell-mediated cytotoxicity (ADCC)?
Inflammatory cells attach to target cells already coated with low concentrations of antibodies via the Fc receptor portion, leading to destruction of the target cells.
44
Name examples of conditions involving ADCC.
HII
Hyperacute transplant rejection, immune reactions against neoplasms, immune reactions against parasites.
45
What characterizes antibody-mediated cellular dysfunction in Type II reactions?
Dysfunction of target cells due to antibodies directed against receptors present on these cells.
46
Provide examples of conditions involving antibody-mediated cellular dysfunction.
Myasthenia gravis (acetylcholine receptor antibody)
Graves' disease (TSH receptor antibody)
Pernicious anemia (gastric parietal cell antibody).
47
Grave's disease
TSH receptor antibody
47
Myasthenia gravis
acetylcholine receptor antibody
48
What characterizes Type III hypersensitivity reactions?
Antibody (IgG) binds to soluble antigen to form an antigen-antibody complex.
49
Type III
Immune Complex mediated
50
What happens to the antigen-antibody complex in Type III reactions?
The complex is deposited on vessel walls, often in the joints or kidneys.
51
What is the consequence of the deposition of antigen-antibody complexes in Type III reactions?
It initiates an inflammatory reaction, leading to tissue damage.
52
Provide examples of conditions resulting from Type III hypersensitivity reactions.
Vasculitis (inflammation of blood vessels)
Nephritis (inflammation of renal glomeruli)
Arthritis, such as rheumatoid arthritis (inflammation of joint spaces)
Arthus reaction, systemic lupus erythematosus (SLE) (inflammation of subcutaneous tissue)
53
Vasculitis
inflammation of blood vessels
54
Nephritis
inflammation of renal glomeruli
55
Arthritis
eg.rheumatoid arthritis
inflammation of joint spaces
56
Arthus reaction
systemic lupus erythematosus (SLE) (inflammation of subcutaneous tissue)
57
SLE
systemic lupus erythematosus
58
What characterizes Type IV hypersensitivity reactions?
Inappropriate or excessive reactions initiated by specifically sensitized T lymphocytes.
59
What types of T lymphocytes are involved in Type IV reactions?
T helper cells (CD4+) or T cytotoxic cells (CD8+).
60
Is antibody production involved in Type IV hypersensitivity reactions?
No
61
How is the antigen presented to T lymphocytes in Type IV reactions?
Antigen is presented to T lymphocytes by antigen-presenting cells.
62
What happens when T lymphocytes are activated in Type IV reactions?
Activated lymphocytes release mediators (lymphokines) to recruit and activate lymphocytes, macrophages, and fibroblasts, resulting in severe tissue injury and fibrosis.
63
Describe Delayed Type Hypersensitivity (DTH) reaction.
Mediated by CD4+ helper T cells, DTH releases mediators to cause inflammation and tissue damage with fibrosis.
64
What characterizes Cell-Mediated Cytotoxicity in Type IV reactions?
Mediated by CD8+ T cells, it causes direct cell killing and tissue damage.
65
What is the Tuberculin Skin Test also known as?
Mantoux reaction.
66
Describe the procedure of the Tuberculin Skin Test.
It involves intradermal injection of tuberculous antigen into a previously sensitized individual.
67
What indicates a positive test result in the Tuberculin Skin Test?
The appearance of a local area of erythema and induration within 8-12 hours, peaking by 24-72 hours.
68
Explain the mechanism behind the positive test result of the Tuberculin Skin Test.
The tuberculin antigen is picked up by antigen-presenting cells (APCs) and presented to memory T helper (CD4+) cells.
CD4+ T cells then secrete mediators to activate macrophages, causing inflammation, which manifests as a "red" elevated area.
69
How does a delayed type hypersensitivity reaction occur in response to poison ivy?
Contact with poison ivy leads to sensitization, and upon subsequent exposure, memory T cells react with the antigen, leading to a delayed inflammatory response characterized by itching, redness, and blister formation
70
Describe the initial interaction between the virus and liver cells in viral hepatitis infection.
The virus attaches to the surface of liver cells but does not enter the cell, thus avoiding detection by the immune system.
71
How are viral antigens presented to the immune system in viral hepatitis infection?
Viral antigens are displayed by the MHC I molecules on the surface of liver cells, inducing proliferation of CD8+ cytotoxic T cells.
72
What is the role of CD8+ cytotoxic T cells in viral hepatitis infection?
CD8+ cytotoxic T cells directly kill infected liver cells either by releasing enzymes that activate the cell's own death signal (apoptosis) or by releasing mediators that recruit and activate macrophages, leading to additional inflammation and fibrosis (cirrhosis).
73
What other phenomenon can occur in viral hepatitis infection involving activated macrophages?
What other phenomenon can occur in viral hepatitis infection involving activated macrophages?
74
What are the immunogenic molecules that stimulate the rejection of transplanted organs?
Histocompatibility leukocyte antigens (HLA).
75
Why is it important for the recipient and donor to have closely matched HLA?
For optimal survival of the graft.
76
What triggers graft rejection?
Graft rejection occurs when the host recognizes the grafted tissue as foreign.
77
Describe the complexity of the rejection process.
Rejection is a complex process involving both cell-mediated immune reaction (Type IV) and circulating antibodies (Type II - antibody-dependent cell-mediated cytotoxicity (ADCC) reaction).
78
When does hyperacute rejection typically occur after transplantation?
within minutes or hours after transplantation or may even be recognized on the operating table.
79
What is the cause of hyperacute rejection?
It is due to an antigen-antibody reaction at the vascular endothelial level.
80
When does acute rejection occur after transplantation?
It occurs within days of transplantation in the untreated recipient or may appear suddenly months or even years after the termination of immunosuppression.
81
What mechanisms are involved in acute rejection?
Acute rejection involves both cell-mediated and humoral mechanisms of tissue damage.
82
What characterizes chronic rejection?
Chronic rejection is dominated by vascular changes, interstitial fibrosis, and loss of parenchyma.
83
Pernicious anemia
gastric parietal cell antibody
84
When does acute rejection occur after transplantation?
It occurs within days of transplantation in the untreated recipient or may appear suddenly months or even years after the termination of immunosuppression.
85
What mechanisms are involved in acute rejection?
Acute rejection involves both cell-mediated and humoral mechanisms of tissue damage.
86
What characterizes chronic rejection?
Chronic rejection is dominated by vascular changes, interstitial fibrosis, and loss of parenchyma.
87
Chronic Rejection:
EXPLAIN
Long-term process where the body's immune system gradually damages the transplanted organ over time.
88
Chronic Rejection:
KEY FEATURES
Gradual damage to the organ's blood vessels.
Buildup of scar tissue (fibrosis).
Loss of normal functioning tissue (parenchyma).
89
Chronic Rejection:
OUTCOME
Can lead to the failure of the transplanted organ over time.
