Immunology Flashcards
What is a transplantation between different individuals of the same species, and between different species? (2)
Allograft same species
Xenograft different species
What are risks of immunosuppression? (4)
- Increase risk of getting infection both conventional infections and opportunistic, or activation of dormant pathogen such as TB
- Increase risk of malignancy
- Cardiac toxicity
Transplantation between different individuals of the same species is called: (1 mark)
Allograft
Transplantation between individuals of the different species is called: (1 mark)
Xenograft
Name two clinically useful drugs that are used to help prevent graft rejection, and state how they work (4 marks) / What are 2 drugs used in transplantation and their mechanism of action? (4)
- Tacrolimus - inhibit t lymphocyte signal transduction (CNI inhibitor)
- Cyclosporin - inhibit t lymphocyte signal transduction (CNI inhibitor)
- Rapamycin - inhibit t lymphocyte signal transduction (mTOR inhibitor)
- Azathioprine - antiproliferative agent - purine synthesis inhibitor
- Corticosteroids
Name two common complications that usually arise from using these drugs, and name an example for each (2 marks)
- Tacrolimus - side effects include cardiac damage, nephrotoxicity, lung damage, increased chance of malignancy
- Cyclosporin - side effects include convulsions, pancreatitis, kidney and liver dysfunction
- Rapamycin - side effects include lung toxicity, DM
- Azathioprine - side effects include nausea, vomiting anaemia
- Corticosteroids - cushing’s
- All would cause decreased immune system so increased chance of infection and cancer
Name 3 things that could cause anaphylactic shock (5)
Food e.g. peanuts, insect sting e.g. wasp, medication e.g. penicillin
what is atopy (2)
Tendency to produce abnormally high IgE responses to otherwise harmless foreign substances
Genetic tendency to develop allergic diseases, e.g. rhinitis, asthma, eczema
Explain what happens during an anaphylaxis. You may use diagrams.
Allergen –> severe generalised allergic reaction due to generalised mass degranulation of IgE sensitised mast cells
• Vasodilation and cardiovascular collapse
• Respiratory effects are bronchospasm and laryngeal oedema
• Skin effects are vasodilation, erythema, urticaria and angioedema
What are the three types of kidney transplant rejection? Give their type, onset and cause.
Hyperacute –> mins/hours –> due to pre-existin B cell antibodies eg. wrong blood type transfused
Acute –> days –> due to B/T cells –> body develops antibodies to foreign body for transplant etc. –> tissue destroyed
Chronic –> months/years –> B/T cell mediated
Explain/describe the immunological occurrences in asthma (3)
Sensitisation to antigen. Antigen taken by dendritic cells to Th 2 cells - release IL-5 (activates eosinophils) and IL-4 and IL-13 to cause IgE production. Reexposure to antigen - crosslinks IgE on mast cell causing degranulation - histamine release, leukotriene production, prostanoid production. Results in increased permeability of capillaries -> oedema. Also bronchoconstriction and increase mucus production
Give the 3 main clinical features of asthma (3)
- Difficulty breathing
- Chest tightness
- Wheezing
Give 4 treatments in managing asthma in order of severity (4)
1- Short acting B2 agonist eg. salbutamol
2- Low dose of inhaled corticosteroids eg. budesonide
3- Long acting B2 agonist and high dose inhaled corticosteroids
4- Oral corticosteroids eg. prednisone
Name 3 autoimmune diseases and state the organ they affect (3)
- Hashimoto’s disease – thyroid
- rheumatoid arthritis - joints(particularly small joints)
- T1DM - pancreatic B cells
- Graves - thyroid, pernicious anaemia - stomach
Differences between type 2 and type 3 hypersensitivity reactions (2)
Type 2 - insoluble receptors, antibody mediated
Type 3 - soluble receptors, immune complex mediated
Name 4 ways in which pathogenic infections can predispose to hypersensitivity reactions/allergy (2)
Can reduce ignorance through damage- expose immunologically privileged sites
Immune shift/deviation e.g. Th1 to th2 response
Increased costimulatory molecules- pro inflammatory
Molecular mimicry of self: If pathogen expresses molecule that is very similar to self molecule then induces immune response against self
Define hypersensitivity
Hypersensitivity reactions are inappropriate immune responses mounted against harmless foreign antigens, autoantigens or alloantigens
Explain the mechanism of T1 hypersensitivity + give an example.
Type I = immediate, IgE mediated. Need sensitisation - primary exposure to form IgE. Then secondary exposure antigen can cross link IgE -> mast cell degranulation, eosinophil and basophil recruitment. Anaphylaxis
Explain the mechanism of T2 hypersensitivity + give an example.
Type 2 = Ab-dependent cytotoxicity. Tissue damage. e.g. Pernicious anemia. Hemolytic anemia.
Explain the mechanism of T3 hypersensitivity + give an example.
Type 3 = Immune complex. Antigen-antibody complexes form in blood - deposition in tissue. Complement, cell activation/recruitment, activation of other cascades Causes vasculitis. SLE
Explain the mechanism of T4 hypersensitivity + give an example.
Type 4= T-cell, delayed. Transient/persistent antigen causes T cell activation of macrophages, CTLs causes tissue damage - dependant on TNF alpha. Th1 or CTLs release TNFa. Contact dermatitis, chronic graft rejection
Give an example of a disease for type II and III and state what antigen is targeted(4)
Type II - Graves - TSH receptor, with Anti-ACh R, Pernicious anaemia - intrinsic factor
Type III - SLE - dsDNA, nucleosome. Antibodies in SLE are anti dsDNA, anti cardiolipin –> cardiolipin is antigen
What is tolerance? In what kind of immune cells does it occur?
Tolerance - Defined as the acquired inability to respond to an antigenic stimulus
Involves cells of the acquired/adaptive immune system
What are central and peripheral tolerance?
Central - lymphocytes that respond to self antigens in the bone marrow for B cells or in the thymus for T cells will undergo apoptosis so they are not exposed to the body. T cells exposed to MHC - if can’t detect it or detect it too strongly -> apoptosis. B cell exposed to multivalent molecule - has many of bodies antigens - if generates response -> apoptosis. Crosslinking of surface immunoglobulin by polyvalent antigens expressed on bone marrow stromal cells facilitates deletion
Peripheral - anergy - need costimulation to produce response
What are two differences between central and peripheral tolerance?
Central tolerance occurs during lymphocyte development, involves T cell selection in the thymus and B cell selection in the bone marrow. Peripheral tolerance - mechanisms to generate tolerance once mature lymphocytes have been developed - involves anergy, immune privilege and regulation
2 mechanisms by which failures in tolerance can lead to autoimmune disease.
Failure in tolerance - centrally - e.g. mutation of transcription factor AIRE - important in expression of ‘tissue-specific’ genes in thymus - involved in negative selection of T cells results in APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy) - affects endocrine glands.
Failure of tolerance - peripherally IPEX - costimulation of self antigen. Trauma to privileged site - increase amount of antigen - immune attack. Defect of T reg
Define each type of hypersensitivity briefly
- Type 1 immediate hypersensitivity
- Type 2 antibody-dependent cytotoxicity
- Type 3 immune complex mediated
- Type 4 delayed cell mediated
