• Hypersensitivity
• Lecture (11)
• Dr.Baha, H. AL-Amiedi
• Ph.D. Microbiology
Hypersensitivty
In immunity focus of attention is antigen (Killing , neutralization of toxin).
in hypersensitivity focus of attention is
what happens to host as a result of immune reaction.
Some forms of’ immune reaction can produce sever and occasionally Fatal results. This are known hypersensitivity.
• Mechanisum:
• The mechanisum of hypersensitivity is that reactions that appear within minutes are mediated by freely diffusible antibody molecules ( immediate type).
• The other type is slow evolving responses that are mediated by sensitized T- lymphoeytes. This cell mediated Hypersensitivity(delayed type)
• Coombs and Gell Classification (1969 ) They are classified hypersensitivity reaction into (4) types on the basis of pathogenesis .It is widely used:
Antigens (red dots) from inhaled pollen are ingested and presented by macrophages to T cells. Activated T cells produce cytokines leading to the production of IgE, which binds to receptors on mast cells(in tissue) and basinophiles in (circulation) causes the release of histamine, which is responsible for allergy symptoms. Onset is usually within minutes of contact with antigen.
• a type of antibody called IgE binds to the allergen causing mast cells to produce chemicals called histamines. Common symptoms include:
– runny nose and itchy, watery eyes, with repeated exposure resulting in a more rapid onset of symptoms
• treatments
– antihistamines are given to counteract the histamines
– shots containing low doses of an allergen can help a person to become desensitized to that specific antigen
Type II hypersensitivity –(cytotoxic) immune-mediated destruction of red blood cells
Drug (p=penicillin) modified red blood cells induce the production of antibodies, because the bound drug makes them look foreign to the immune system. When these antibodies are bound to them, the red blood cells are more susceptible to lysis or phagocytosis. Onset is dependent on the presence of specific antibodies.
• Antibody directed at cell surface antigens activates the Complement
• to damage the cell cause destruction of cell in mismatched blood transfusion or transplanted tissues or hemolytic disease under rhesus
• in compatibility, druge such as penicillin . Quinine attach to surface of Red cell and initiate antibody formation such antibodies (lgG) may then combine with resulting hemolysis.
Type III hypersensitivity – immune complex formation and deposition
Immune complexes of antigen (red dots) and antibody form in target organ
Immune complexes activate complement (green dots- C3a, C4a, and C5a), and mast cells (yellow cell) degranulate.
Inflammation and edema occur, and organ is damaged
• Immune complex or toxic complex e.g.
• Arthus reaction, serum sickness ..etc. In this reaction IgG & IgM and
• Complement take part,it is known as immune complex- mediated hypersensitivity Involve immediate Antibody-mediated (IgG& 1gM ) response soluble proteins, occurs in response to persistent exposure to weakly imm unogenic antigens.
• Antigens may be self components, leading to autoimmume diseases
Type IV hypersensitivity – delayed-type or contact
Antigen (red dots) are processed by local APCs
T cells (blue cells) that recognize antigen are activated and release cytokines
Inflammatory response causes tissue injury.
Antigen is presented by APCs to antigen-specific memory T cells that become activated and produce chemicals that cause inflammatory cells to move into the area, leading to tissue injury. Inflammation by 2-6 hours; peaks by 24-48 hours.
• it is delayed type of hypersensitivity in which T-cells, lymphokine and macrophages take part e.g. tuberculin type and contact determintis, It is one of aspect cell mediated immunity .The antigen activates specifically macrophages &sensitized T-Cell leading to secretion of lymphokines. Locally the reaction is manifested by infiltration with mononuclear cell these reactions have the following
• characters,
• Antigen stimulus is necessary. Induction period 7-days a sensitive subject reaction occurs on exposure to specific antigen .e.g. tuberculin reaction.
• Delayed hypersensitivity is transsferted by cells from lymphoid tissue, peritoneal exudates or blood lymphocytes. Two type delayed
• Classical or tuberculin type
• Granulomatous reactions.
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .