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Month: February 2018

Antibody Dependent Cell-Mediated Immunity

Posted on February 26, 2018 in Uncategorized

Hypersensitivity reactions mediated by antibodies fall into different types. These are: anaphylactic reaction, cytotoxic hypersensitivity, Immune complex mediated tissue damage, T-Cell-mediated hypersensitivity, stimulatory hypersensitivity and antibody dependent cell-mediated cytotoxic mechanism (ADCC). What are they?

Type 1: Anaphylactic reaction

Initial introduction of the antigen (e.g, penicillin) leads to the production of cytotoxic antibodies (mainly IgE) in sensitive persons. These are attached to the surface of mast cells.

On subsequent exposure, the antigen reacts with the preformed antibodies, causing mast cell degranulation and release of histamine serotonin, and slow reacting substance (SRSA). This may lead to asthma due to broncho-constriction, or anaphylactic shock due to wide-spread capillary dilatation.

Allergens such as pollens, house dust and fungi react with cell bound IgE of the respiratory tract leading to bronchial asthma or hay fever. Allergens from food may cause urticaria.

Type I hypersensitivity reaction occurs within 30 minutes of exposure to the allergens. Such reaction can be abolished by drugs like adrenaline and disoduim cromoglycate which prevent the release of histamine. Antihistamines compete with the released histamine for effector sites. Repeated introduction of the allergen in small doses results in hyposensitization.

Type II: Cytotoxic hypersensitivity

Certain drugs may complex with membrane proteins of blood cells leading to production of auto-antibodies. These antibodies can lyse the blood cells through the action of complement. Hemolytic anemia caused by alpha methyl dopa, agranulocytosis produced by amidopyrine and thrombocytopenia induced by chlorothiazides are examples of this mechanism.

Type III: Immune complex mediated tissue damage

The continued presence of antigen causes persistent antibody production. Antigen antibody complexes form and circulate in the blood. These heavy molecules are entrapped in the blood vessels, renal glomeruli, lungs, skin and joints.

Complement system is activated through the alternate pathway. The complement degradation products attract polymorphs and macrophages and an inflammatory reaction sets in with resultant damages to the tissues. Platelet aggregation occurs and these microthrombi lead to vascular occlusion and ischemia. If the antibody is in excess, the complexes are rapidly precipitated and tend to be localized at the site of entry of antigen. This leads to Arthus type reaction. If an antigen is injected intradermally into a hyper-immuned animal, erythema and edema occur at the site of the injection.

This reaction reaches a peak in 3-8 hours, and is referred to as intermediate type skin reaction. Farmer’s lung is the classical example of localized type III reaction. On the other hand, if antigen is in excess, soluble complexes are formed which precipitate in all tissues, giving rise to the serum sickness type of reaction. The lumpy granular precipitates seen in renal glomeruli in post-streptococcal glomerulonephritis are due to systemic type III reaction.

Type IV: T-cell-mediated hypersensitivity reaction

This is also called delayed type hypersensitivity in which a slow erythematous indurated lesion develops after an intradermally injected tuberculin (or similar antigen) on an individual.

Stimulatory hypersensitivity

Thyroid cells are normally stimulated by TSH through a membrane associated receptor. The long acting thyroid stimulator (LATS) which is an antibody against some components if the receptor also produces TSH like activity but it is more prolonged. The continued stimulation of LATS leads to hyperthyroidism. Similarly, anti-lymphocyte globulin is stimulatory to lymphocytes in appropriate conditions.

Type VI: Antibody dependent cell-mediated cytotoxic mechanism (ADCC)

This mechanism does not require complement activity. The effector cells are neither T nor B cells but are called K cells. The specificity of this reaction resides in the antibody molecule. Only very small amounts of antibody are required to produce this reaction and therefore this mechanism is effective in areas where antibody concentration may be minimal, e.g, at the site of solid tumors. The full significance of this mechanism has not been known.

Oral Sex and Sperm Antibodies

Posted on February 19, 2018 in Uncategorized

Ladies, if you’re in the habit of ingesting sperm, get out of the habit today. Experts in the field of immunological infertility have found evidence suggesting that women who swallow their partners’ sperm may form antibodies to the sperm. In a sense, swallowing the sperm is synonymous with being inoculated with it, and you could wind up giving yourself a sperm vaccine!

How is this possible?

When the sperm is introduced into the digestive tract, the immune system sees it as a foreign invader, forms antibodies to it, and kills it off. Later, when the same sperm shows up in the cervical canal, the immune system gets confused and attacks and kills the sperm on the spot, preventing conception.

The more sperm you swallow, the more antibodies you create, so a single episode of ingesting sperm will most likely not affect your fertility. In addition, since the antibodies are created in response to one specific partner’s sperm, past episodes of sperm swallowing with other partners should not cause your body to form antibodies to your current partner’s sperm.

Men often ingest their own sperm when they perform cunnilingus after intercourse with their female partners. In this case, past episodes of this with other partners can affect your fertility today. To avoid swallowing your own sperm, always wash your penis carefully after sex. When a male forms antibodies to his own sperm, the antibodies may even destroy the sperm before they leave his body.

Finally, women who have anal sex with their partners should avoid getting sperm inside their rectums, which can also cause their bodies to create sperm antibodies. Anal sex may cause the tissue inside the rectum to tear, allowing the sperm easy access into the bloodstream, triggering the immune system to create antibodies.

Bear in mind that this theory is still in the research phase and has not yet been absolutely proven! Nevertheless, if it’s true, it could be a powerful piece of preventive medicine for millions of couples.

Antiphospholipid Antibody Syndrome – Is This the Cause of All Autoimmune Diseases?

Posted on February 11, 2018 in Uncategorized

Antiphospholipid antibody syndrome (also APS, phospholipid antibody syndrome, or Hughes syndrome) is an autoimmune disorder, which means that the body’s immune system produces antibodies which attack the normal healthy cells. These antibodies called antiphospholipids, can cause blood clots (usually in leg veins, brain), pregnancy complications, loss of consciousness, stroke, or heart attack. Other signs of this illness may include: rashes, migraines, heart problems, and bleeding.

Antiphospholipid antibody syndrome – two basic types

There are two types of the syndrome: primary (if there are no other autoimmune diseases present) and secondary (if another autoimmune disease is present, such as lupus for example). When the disease is secondary, the cause is always the primary autoimmune disorder.

If the APS is primary, the cause is not always known. It is suspected to be a combination of: genetics (having a relative with antiphospholipid antibodies), infections (syphilis or hepatitis C), and medications (such as hydralazine for high blood pressure) that may trigger the disease.

Antiphospholipid antibody syndrome – conventional treatment approaches

The main goal of the treatment for the condition is to prevent clotting by thinning the blood. Treatments used for this are:

  • Anticoagulants, such as heparin, warfarin, and even aspirin are used as blood thinners
  • Corticosteroids (mainly prednisone) are used to suppress the overactive immune system and reduce inflammation.
  • Intravenous gamma globulin treatment may be prescribed during pregnancy, but it has the same efficacy levels as aspirin and heparin.

Antiphospholipid antibody syndrome – rare complications

Catastrophic antiphospholipid syndrome is rare complication of antiphospholipid antibody syndrome, in which many blood vessels are affected, as well as many organs (brain, heart, skin, lungs etc.). The treatment involves blood thinners, corticosteroids and plasma exchange therapy.

Other more common complications

  • Stroke – due to the reduced blood flow to the brain.
  • Kidney failure – because of the decreased blood flow to the kidneys.
  • Pregnancy complications – miscarriages, fetal death, premature birth; or high blood pressure during pregnancy.
  • Lung problems – pulmonary embolism or high blood pressure in the lungs.
  • Cardiovascular damage – due to the blood clots in the whole body, which may cause damage to the leg veins and as a result of blood not being able to reach the heart, different heart problems, including a heart attack.

Blood tests:

Antiphospholipid antibody syndrome and the presence of antiphospholipid antibodies can be detected with certain blood tests, which are usually repeated to complete the diagnosis. These antibodies can also be found in people who don’t develop antiphospholipid antibody syndrome, most likely caused by some infectious diseases (bacterial, viral or by a parasite), or certain drugs (antibiotics, cocaine, etc.).

This condition is now pinpointed as one of the main potential culprits of a number of autoimmune diseases, but some recent advances in the field of autoimmune disease research offer new found hope to people afflicted by this life-altering condition.

You can learn more by visiting the home page of the protocol as well as get a more detailed image about the antiphospholipid antibody syndrome.