Transplant rejection
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Rejection is a complex process where the recipient's immune system attacks the transplanted organ or graft as foreign. It involves both cell-mediated and antibody-mediated immunity. There are three main types of rejection: hyperacute rejection which occurs within minutes/hours due to pre-existing antibodies, acute rejection within months due to an immune response, and chronic rejection over longer periods due to inflammation. Preventing rejection requires immunosuppressive drugs or techniques to block co-stimulatory signals needed for an immune response.
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1. Transplant rejection occurs when the recipient's immune system attacks the transplanted organ or graft, recognizing it as foreign. It can involve cell-mediated immunity or circulating antibodies.
2. Graft versus host disease occurs when immune cells from the donor engraft in the recipient and attack the recipient's body, seeing it as foreign. It is a risk for allogenic stem cell or solid organ transplants from a donor.
3. Treatment for rejection and GVHD involves immunosuppressive drugs like steroids, ATG, mycophenolate, and antibodies targeting immune cells and cytokines.
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HYPERSENSITIVITY REACTIONS Immunology k
Type I hypersensitivity reactions are immediate and antibody-mediated. Antigens bind to IgE antibodies on mast cells and basophils, causing the release of inflammatory mediators like histamine. This leads to conditions like anaphylaxis, food allergies, and asthma. Type II reactions are also antibody-mediated and cytotoxic, where antibodies bind to antigens on cell surfaces and recruit complement or immune cells to cause cell lysis. Type III reactions involve immune complex deposition in tissues, activating the complement system and recruiting neutrophils, which cause inflammation and tissue damage. Type IV reactions are cell-mediated and delayed, involving T cells and cytokines that activate macrophages to cause tissue damage.
Hypersensitivity by Dr. Rakesh Prasad Sah
Hypersensitivity, also known as allergy, refers to excessive or inappropriate immune responses that damage tissues. There are four main types of hypersensitivity reactions:
1. Type I are immediate hypersensitivity reactions mediated by IgE antibodies, as seen in allergic reactions like anaphylaxis.
2. Type II involve IgG and IgM antibodies binding to cells, leading to cell damage through phagocytosis or complement activation as seen in hemolytic disease of newborns.
3. Type III are immune complex-mediated reactions where antigen-antibody complexes deposit in tissues, activating complement and attracting inflammatory cells, seen in conditions like serum sickness.
4. Type IV are delayed hypersensitivity reactions mediated
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This PPT is made by two student of K.D.dental college, mathura, U.P, India......this was a assignment given to them on IMMUNE RESPONSE
patho3.pptx
This document provides an overview of HIV/AIDS, including its classification, transmission, epidemiology, virology, pathogenesis, and treatment. Key points include:
- HIV is a lentivirus that infects CD4+ cells and integrates into the host genome. It has high genetic diversity and can lie dormant for years.
- HIV is transmitted sexually, through blood exposure, or mother-to-child. Factors like behavior patterns, condom use, and availability of treatment impact spread.
- HIV evades the immune system through rapid mutation, hiding in sanctuaries, and immune activation leading to exhaustion. This allows the virus to persist despite immune responses.
- HIV causes
Pathology Of AIDS
AIDS is caused by the HIV virus, which damages immune cells called CD4+ T cells. This leaves the body vulnerable to opportunistic infections and cancers. It is transmitted via bodily fluids like blood, semen, vaginal fluid and breast milk. While treatments can slow the virus, there is currently no cure. Prevention methods focus on safe sex practices, needle safety, blood screening and education.
Immunopathology
There are two main types of immunity: innate and adaptive. Innate immunity provides initial defense through barriers, phagocytes, and proteins. Adaptive immunity has cellular and humoral components, mediated by T and B lymphocytes, which provide stronger, antigen-specific responses. Hypersensitivity reactions are caused by immune responses against harmless antigens, and include four types. Type I is immediate and antibody-mediated. Type II involves antibody and complement attack of cells. Type III occurs when immune complexes deposit in tissues. Type IV is delayed and cell-mediated. Disorders can also result from immune deficiencies or reactions against self.
immunity and Hypersensitivity.ppt
This document discusses different types of hypersensitivity and immune responses. It covers:
1. The four main types of hypersensitivity reactions (Type I-IV) based on their immune mechanisms, examples of each type, and their characteristic features.
2. Details on Type I immediate hypersensitivity and anaphylaxis, including primary and secondary mediators, mast cell activation, and atopic susceptibility.
3. Type II antibody-mediated hypersensitivity, examples like hemolytic anemia, and mechanisms of tissue damage.
4. Type III immune complex-mediated hypersensitivity, examples like SLE, and mechanisms of inflammation and tissue damage.
5. Type IV delayed hypersensitivity, using tuberculosis as an
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TRANSPLANTATION IMMUNOLOGY
Transplantation involves transferring organs, tissues or cells from one part of the body to another or between individuals. Compatibility of immune molecules like HLA antigens, ABO blood groups, MIC antigens and KIR determines transplant success. Major histocompatibility complex (MHC) molecules control immune response and are targets in transplant rejection. Incompatibility can lead to hyperacute, acute cellular or chronic rejection as well as graft-versus-host disease. Immunosuppressive agents like corticosteroids, calcineurin inhibitors and monoclonal antibodies are used to suppress anti-graft immune responses.
Acute and Chronic inflammation & Wound Healing
This document discusses acute and chronic inflammation and wound healing. It defines inflammation and describes its purpose. There are two main types: acute and chronic inflammation. Acute inflammation is short-term and involves chemicals like toll-like receptors and arachidonic acid metabolites. Chronic inflammation is long-lasting and characterized by lymphocytes and macrophages. It can lead to outcomes like scarring, amyloidosis, or neoplastic transformation. Wound healing involves regeneration or repair through granulation tissue formation and is affected by factors like infection, nutrition, and vascular disease. Abnormal wound healing can result in dehiscence or scarring.
Inflammation in dentistry-SEMINAR
The document provides an overview of inflammation, including its definition, etiology, cardinal signs, types (acute and chronic), vascular and cellular events in acute inflammation, mediators, regulation, inflammatory cells, factors affecting acute inflammation, and the fate of acute inflammation. It also discusses chronic inflammation, granulomatous inflammation, comparing acute and chronic inflammation, and dental implications including pulpal infections, periapical infections/inflammation, gingival inflammation, and periodontal inflammation.
Immunopathology lecture 2+3 ,final
The document discusses different types of immune disorders:
1. Hypersensitivity reactions (allergies) are caused by an exaggerated immune response upon re-exposure to an antigen and are classified into four types.
2. Autoimmune diseases occur when the immune system attacks the body's own tissues.
3. Immunodeficiency diseases result from inadequate immune response.
4. Amyloidosis involves abnormal protein buildup in tissues.
Primary immune dificiency
1. A secondary immune response occurs upon reexposure to an antigen and results in a faster and stronger response than the primary response due to memory cells.
2. The secondary response has a very short or negligible lag phase and the antibody concentration increases much more rapidly than in the primary response, reaching levels 100-1000 times higher.
3. Memory B and T cells generated during a primary response enable a rapid secondary response through faster activation, greater sensitivity, and production of more effective antibodies.
Hypersensitivities
hypersensitivity Undesirable reactions produced by the normal immune system. Hypersensitivity is an exaggerated immune response that results in tissue damage and is manifested in the individual on a second or subsequent contact with an antigen. Hypersensitivity reactions can be classified as either immediate or delayed. Obviously immediate reactions appear faster than delayed ones, but the main difference between them is the nature of the immune response to the antigen.
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Antibody mediated rejection pathology histopathology
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Transplant rejection
- 2. Rejection is a complex process in which “recepient immune system recognize the graft as foreign and attacks it”. It involves 1. Cell mediated immunity 2. Circulating antibodies
- 3. It is caused by T-cell mediated reactions. Destruction of grafts occurs by 1. CD8+ CTLs 2. CD4+ helper cells Delayed hypersensitivity is triggered by CD4+ helper cells. 2 pathways 1. Direct pathway 2. Indirect pathway
- 5. It is called humoral rejections. 2 types 1. Hyperacute 2. Acute HYPERACUTE: Presence of preformed antidonor antibodies. Transplant rejection has already occurred.
- 6. ACUTE: Initial exposure to class I&II HLA antigens. Antibodies causes injury by 1. Complement dependent cytotoxicity 2. Inflammation 3. Antibody dependent cell mediated cytotoxicity.
- 7. Rejection reactions 1. Hyperacute 2. Acute a. cellular b. humoral 3. Chronic
- 8. Occurs within minutes or hours after transplantation. Kidney becomes 1. Cyanotic 2. Mottled 3. Flaccid Immunoglobulin and complement deposition occurs. Neutrophils accumulate leading to occlusion of capillaries & fibrinoid necrosis.
- 10. Cellular – mononuclear cell infiltrate Humoral – vasculitis ACUTE CELLULAR: Seen within initial months after transplantation. Mononuclear cells accumulates in glomerular and peritubular capillaries leading to FOCAL TUBULAR NECROSIS. Treatment – cyclosporin.
- 12. Also known as rejection vasculitis. Necrotizing vasculitis characterised by intimal thickening. Presence of complement breakdown product C4d – indicator of humoral rejection. Treatment – B cell depleting agents.
- 16. Immunosuppressive agents 1. Cyclosporin 2. Azathioprine 3. Steroids 4. Rapamycin 5. Monoclonal antibodies.
- 17. ANOTHER METHOD: Prevention of host T cells from receiving co-stimulatory signals (B7- 1&2) from dendritic cells. DISADVANTAGES: EBV induced lymphoma HPV induced squamous cell carcinoma Kaposi sarcoma
- 18. Hematopoietic stem cell transplants are used for 1. Hematological malignancy 2. Aplastic anemia 3. Thalassemia 4. Non hematological cancers PROBLEMS: 1. Immunodeficiency 2. GVH disease
- 19. Occurs in any situation in which “immunologically competent cells or their precursors are transplanted to immunologically crippled recipients and the transferred cells recognize allo-antigens in the host”. It may be 1. Acute 2. Chronic
- 20. Days to weeks after allogenic bonemarrow transplantation. Clinical features 1. Generalised rash 2. Jaundice 3. Ulceration of gut 4. Bloody diarrhea
- 21. Follow acute syndrome or occur insidiously. Clinical features 1. Cutaneous injury 2. Cholestatic jaundice 3. Esophageal strictures 4. Depletion of lymphocytes It is a life threatning condition. Treatment – bonemarrow transplants.