describe immune mechanisms involved in d 4 diff. types of HYPERSENSITIVITY?
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Type-I : Anaphylactic\nAntibody: IgE\nAntigen: exogenous\nResponse time 15-30mins\nAppearance: Weal & flare\nHistology: Basophil & Eosinophil\nTransferred with: Antibody\nEg,: Allergic asthama, hay fever\n\nType-II : Cytotoxic \nAntibody: IgG, IgM\nAntigen: cell surface\nResponse time mins-hrs\nAppearance: lyses & necrosis\nHistology: Antibody & complement\nTransferred with: Antibody\nEg,: Erythroblastosis fetalis, Goodpastures syndrome\n\nType-III : Immune complex mediated\nAntibody: IgG, IgM\nAntigen: soluble\nResponse time 3-8hrs\nAppearance: erythematic, edema, necrosis\nHistology:  Complement & Neutrophils\nTransferred with: Antibody\nEg,: SLE, farmer’s lung disease\n\nType-IV : Delayed type\nAntibody: None\nAntigen: tissue & organ\nResponse time 48-72hrs\nAppearance: erythematic & induration\nHistology:  Monocyte & Lymphocytes\nTransferred with: T-cells\nEg,:  Tuberculin test, poison ivy,granuloma\n\nfor more : http://pathmicro.med.sc.edu/ghaffar/hyper00.htm
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Here's a great site that helps you understand allergies.\n\nhttp://allergies.about.com/od/basics/Allergy_101_Basic_Allergy_Information_and_FAQs.htm
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Not sure if this will help, but check out this paper:\nhttp://www.nature.com/nature/journal/v415/n6871/full/415536a.html\n\nThis is the abstract:\n\nActivation of naive CD4+ T-helper cells results in the development of at least two distinct effector populations, Th1 and Th2 cells1. Th1 cells produce cytokines (interferon (IFN)-, interleukin (IL)-2, tumour-necrosis factor (TNF)- and lymphotoxin) that are commonly associated with cell-mediated immune responses against intracellular pathogens, delayed-type hypersensitivity reactions4, and induction of organ-specific autoimmune diseases5. Th2 cells produce cytokines (IL-4, IL-10 and IL-13) that are crucial for control of extracellular helminthic infections and promote atopic and allergic diseases4. Although much is known about the functions of these two subsets of T-helper cells, there are few known surface molecules that distinguish between them. We report here the identification and characterization of a transmembrane protein, Tim-3, which contains an immunoglobulin and a mucin-like domain and is expressed on differentiated Th1 cells.
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This site should be able to explain it for you....\n\nhttp://www.cancerbacup.org.uk/Cancertype/Lymphomanon-Hodgkins/General/WhatareNHLs
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Pathophysiology: As a group, regardless of etiology, a common pathophysiology exists that begins with acute injury to the pulmonary parenchyma, leading to chronic interstitial inflammation, and ultimately progressing to the common end point of pulmonary fibrosis and tissue destruction. \n\nThe DPLDs typically manifest with the insidious onset of respiratory symptomatology, although onset can be acute and rapidly progressive, as in bronchiolitis obliterans-organizing pneumonia (BOOP) or acute interstitial pneumonitis. \n\nPathologically, all manifest histologically with disease in the interstitial compartment of the lung. The histologic patterns of usual interstitial pneumonitis (UIP), desquamative interstitial pneumonitis (DIP), nonspecific interstitial pneumonitis, hypersensitivity pneumonitis (HSP), lymphocytic interstitial pneumonitis, BOOP, giant cell pneumonitis, and granulomatous pneumonitis are most common and are centered in the alveolar, lobular, and lobar septa, impacting alveoli, small airways, and pulmonary vasculature.
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Innate (non-specific) immunity:\n1) the enzyme lysozyme, which if found in tears and saliva, breaks down cells walls of Gram positive bacteria\n2) skin/mucus provides physical barrier against opportunistic pathogens\n\nAcquired (specific) immunity:\n1) antibodies: most helpful against extracellular pathogens like most bacteria and fungi\n2) T cells: target host cells that are infected by intracellular pathogens like viruses (and a few bacteria)\n3) macrophages: release reactive oxygen intermediates that cause oxidative stress to various bacteria
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CD4 (cluster of differentiation 4) is a surface antigen, a small molecule that is part of certain cells in the body, which helps the cell to communicate with cells around it.\n\nIt is found on all 'T Helper' cells which are a normal and important part of the immune system.  Other cells in the immune system are responsible for picking up foreign molecules in the body, such as viruses and bits of bacteria, and these are then 'presented' to T Helper cells.  The CD4 receptor on the T Helper cells then recognises the molecule and activates the T Helper cell, starting an immune reaction in the body.\n\nT Helper cells are particularly important in fighting viral infections.\n\n\nHIV is a virus that infects CD4 T Helper cells, stopping it's ability to protect the body from infection.  As more and more T Helper cells are destroyed by HIV, the body can no longer prevent dangerous infections, and this is called AIDS.
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Complement mediation needs some amount of energy (created by Glucose utilisation)and so bactiriacidal activity is lower in less controlled diabetics.Complement inactivated serum does not need extra energy.I can not readily explain defference between C3 and  C4.Even plasma cells need effective glucose utilisation for optimal functioning.So IgG and IgA  are in higher quantity.
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the only one i can think of is Inergy
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Through a series of steps called the immune response, the immune system attacks organisms and substances that invade our systems and cause disease. The immune system is made up of a network of cells, tissues, and organs that work together to protect the body.\n\nThe cells that are part of this defense system are white blood cells, or leukocytes (pronounced: loo-kuh-sytes). They come in two basic types (more on these below), which combine to seek out and destroy the organisms or substances that cause disease. \nThe leukocytes circulate through the body between the organs and nodes by means of the lymphatic (pronounced: lim-fah-tik) vessels. (You can think of the lymphatic vessels as a type of highway between the rest stops that are the lymphoid organs and lymph nodes). Leukocytes can also circulate through the blood vessels. In this way, the immune system works in a coordinated manner to monitor the body for substances that might cause problems.A foreign substance that invades the body is called an antigen (pronounced: an-tih-jun). When an antigen is detected, several types of cells work together to recognize and respond to it. These cells trigger the B lymphocytes to produce antibodies. Antibodies are specialized proteins that lock onto specific antigens. Antibodies and antigens fit together like a key and a lock.Once the B lymphocytes have produced antibodies, these antibodies continue to exist in a person's body. That means if the same antigen is presented to the immune system again, the antibodies are already there to do their job.Although antibodies can recognize an antigen and lock onto it, they are not capable of destroying it without help. That is the job of the T cells. The T cells are part of the system that destroys antigens that have been tagged by antibodies or cells that have been infected or somehow changed. (There are actually T cells that are called "killer cells"). T cells are also involved in helping signal other cells (like phagocytes) to do their jobs.\n\nAntibodies can also neutralize toxins (poisonous or damaging substances) produced by different organisms. Lastly, antibodies can activate a group of proteins called complement that are also part of the immune system. Complement assists in killing bacteria, viruses, or infected cells.\n\nAll of these specialized cells and parts of the immune system offer the body protection against disease. This protection is called immunity. Humans have three types of immunity - innate, adaptive, and passive.
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D - it can cause hyperpolarization or depolarization of membrane
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The Cause of Type 1 Diabetes\n\nAutoimmune reactions, in which the body's white blood cells harm its own tissues, cause many diseases including type 1 diabetes, multiple sclerosis, Hashimoto's thyroiditis and arthritis, among others. We don’t known why immune cells target certain organs, and why in type 1 diabetes, only insulin-producing cells are killed.\n\nIn type 1 diabetes, the body's immune T-cells react against beta cells -- the insulin-producing cells in the pancreas -- effectively shutting them down and triggering disease onset.\n\nSo, it is known that type 1 diabetes is caused by the body's immune system turning against cells in the pancreas that produce insulin. What's remained unclear is the target for this immune response.\n\nSome studies report that albumin, the protein in milk, is a causal agent for that immune reaction. Also some theories point toward viruses. The glutamic acid decarboxylase is another molecule that has been believed to be the cause for that reaction.\n\nNow, after eight long years of careful research, scientists believe they've finally pegged insulin as the prime antigen -- immune system target -- responsible for this shutdown.\n\nDr. David A. Hafler, Breakstone professor of neurology at Harvard Medical School guided the research, which appears in the May issue of Nature. Unfortunately, the only way to adequately answer that question in humans is to examine tough-to-obtain pancreatic lymph tissues.\n\n"It took us years to get these tissues, to clone the cells and then to really characterize them and examine their activity," he said. “The results of that effort show that indeed the target -- the cause -- of type 1 diabetes may be T-cell reactivity to insulin," Hafler said.\n\nHis team in Miami has been testing insulin as a potential basis for a vaccine against type 1 diabetes. However, another expert in type 1 diabetes research, Edwin Gale --who is professor of diabetic medicine and head of the department of clinical science at the University of Bristol in England-- cautioned that a potent vaccine against the illness remains a distant goal.\n\nThese findings are very interesting for people with type 1 diabetes, but not for those with type 2 diabetes, since although in both cases the result is hyperglycemia, the causes are different. Reports Health Day News\n\n\nWhat Causes Type 2 Diabetes\n\nType 2 diabetes affects about 200 million people worldwide and has a predicted increase to 300 million by 2025. Also, nowadays more and more children and adolescents are developing Type 2 diabetes, which used affect mostly adults in the past.\n\nRecent studies reveal that genetics, obesity, fetal history, lack of activity, a diet high in fat and stress, all may play a role in the development diabetes.\n\nGenetic studies have shown that the association of some genes is the root of the cause of Type 2 diabetes. A healthy and active lifestyle for the whole family of a person with diabetes is then greatly recommended to protect their children and young people.\n\nLow birth weight has also been associated with Type 2 diabetes. It seems that poor nourishment of the fetus increases the risk of insulin resistance and Type 2 diabetes.\nIf that baby is overfed and becomes overweight during childhood, then the risk is a lot higher.\n\nOn the other hand, stress has been associated with insulin resistance, which leads to Type 2 diabetes. This happens due to the cascade of metabolic reactions that our emergency hormones trigger when we are stressed.\n\nObesity has long been associated with diabetes, as well as the lack of physical activity and a diet high in fat. This is thought to cause a condition called insulin resistance.\n\nWhat is insulin resistance?\n\nInsulin resistance means that your muscles, fat, and liver cells cannot use insulin properly. There can be a lot of insulin circulating, but the cells are incapable of using it to allow glucose entering the cells and be conv
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http://www.google.co.in/search?hl=en&q=multiple+genes&btnG=Search&meta=\n\nhttp://www.newton.dep.anl.gov/askasci/bio99/bio99889.htm\n\nhttp://www.jimmunol.org/cgi/content/full/173/11/6501
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rabies\nYou can be allergic to them.
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The immune system is composed of many interdependent cell types that collectively protect the body from bacterial, parasitic, fungal, viral infections and from the growth of tumor cells. Many of these cell types have specialized functions. The cells of the immune system can engulf bacteria, kill parasites or tumor cells, or kill viral-infected cells. Often, these cells depend on the T helper subset for activation signals in the form of secretions formally known as cytokines, lymphokines, or more specifically interleukins. The purpose of this article is to review the organs, cell types and interactions between cells of the immune system as a commentary on their importance and interdependence on the T helper subset. Such an understanding may help comprehend the root of immune deficiencies, and perceive potential avenues that the immune system can be modulated in the case of specific diseases.
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I don't know if your looking for info specifically on the visual hypersensitivity or just on autism in general. I would recommend contacting the connections center. Dr Gutstein has developed an amazing program. You can get more info at  rdiconnect.com\n\n\nAlso there was a link on the autism research institutes website. Dr Kaplan did some pretty interesting work.
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cytotoxic T cells-helps to kill d antigen through phagocytosis.it takes the help of macrophage,natural killer cells and dendritic cells.or can say kills and removes d antigen or foreign bodies from the body.\n\nhelper T cell-helps the B cell to kill d antigen.\n\nsuppressor T cell as d name suggests supresses the antigen or supresses the disease.