Diseases Caused By Immune Reponses: Hypersenstivity - I


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Rgwbkpkszehveve5inhg 180307 s0 hashmi uzair diseases caused by immune responses hypersenstivity i intro
Diseases Caused By Immune Reponses: Hypersenstivity - I
Lveghqljqmqww4iu9im7 180307 s1 hashmi uzair diseases caused by antibodies
Diseases Caused by Antibodies
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Diseases Caused by T lymphocytes
Ng7gobzsgwcmvvh9dmqr 180307 s3 hashmi uzair type i hypersensitivity
Type I Hypersensitivity
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Type II Hypersensitivity: Introduction
Xpvwztcgq0yrsk1t1opc 180307 s5 hashmi uzair type ii hypersensitivity mechanisms sub 01
Type II hypersensitivity: Mechanisms

Lecture´s Description

Diseases Caused by Antibodies

This Sqadia lecture elucidate about disease caused by immune responses. The body’s immune system can be equally as toxic to foreign organisms as it can to its own tissues. A hyperactive immune system, or having certain over-sensitive types of antibodies, can wreak havoc on the body. An autoimmune disease is a condition in which your immune system mistakenly attacks your body. The immune system normally guards against germs like bacteria and viruses. When it senses these foreign invaders, it sends out an army of fighter cells to attack them. Normally, the immune system can tell the difference between foreign cells and your own cells. In an autoimmune disease, the immune system mistakes part of your body like your joints or skin as foreign. It releases proteins called autoantibodies that attack healthy cells. Fixed antigen has three mechanisms:

1. Opsonization and phagocytosis

2. Complement and Fc receptor mediated inflammation

3. Abnormal physiological responses without cell injury

Diseases Caused by T lymphocytes

Patients with T cell defects can present with a variety of organ specific autoimmune diseases (e.g., type 1 diabetes mellitus in infancy, hypothyroidism, and Addison’s disease) caused by the attack on these organs by the patient’s own immune cells. The basis for these clinical complications is unclear but are thought to be caused by a breakdown in immune tolerance in which a lack of T regulatory cells or the participation of Th17 cells plays a critical role in the pathogenesis of these disorders. Hypersensitivity refers to undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system. Hypersensitivity reactions divided into the following 4 types:

•                     Type I hypersensitivity

•                        Type II hypersensitivity

•                        Type III hypersensitivity

•                        Type IV hypersensitivity

Type I Hypersensitivity

Immediate or anaphylactic hypersensitivity reactions are also called allergy. The reaction takes 15-30 minutes from the time of exposure to the antigen. Sometimes the reaction may have a delayed onset (10-12 hours). Antigens that elicit immediate hypersensitivity reactions are called allergens which includes: pollen, certain foods, insect venom and certain drugs. Some IgE mediated anaphylaxis in response to insect venom, drugs or foods are not associated with atopy. Epinephrine is the drug of choice for systemic anaphylactic reactions: relaxing the smooth muscles and reducing vascular permeability improves cardiac output. Type I hypersensitive reaction begins to subside, mediators released during the course of the reaction often induce localized inflammation called the late-phase reaction.

Type II Hypersensitivity: Introduction

Type II hypersensitive reactions involve antibody-mediated destruction of cells. Antibody can activate the complement system, creating pores in the membrane of a foreign cell. It can mediate cell destruction by antibody dependent cell-mediated cytotoxicity (ADCC). Antibody bound to a foreign cell also can serve as an opsonin. Haemolytic Disease of the new-born is caused by Type II Reactions. Haemolytic disease of the new-born develops when maternal IgG antibodies specific for fetal blood-group antigens cross the placenta and destroy fetal red blood cells. Severe haemolytic disease of the new-born, called erythroblastosis fetalis, most commonly develops when a Rh+ fetus expresses an Rh antigen on its blood cells that the Rh– mother does not express.

Type II hypersensitivity: Mechanisms

Type II hypersensitivity involves IgG or IgM induced damage to self-cells (Cell-surface or Matrix Antigen). Either IgG or IgM is made against normal self-antigens- failure in immune tolerance or a foreign antigen resembling some molecule on the surface of host cells enters the body and IgG or IgM made against that antigen then cross reacts with the host cell. Clinical manifestations in association with haemolytic anaemia linked to blood transfusions may occur due to massive haemolysis due to antibody and complement system. Symptoms include fever, low haemoglobin, increased bilirubin, mild jaundice, and anaemia. Free haemoglobin is usually not detected in the plasma or urine in these reactions because RBC destruction occurs in extravascular sites.

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