Reply #37: Immunology 101

[HysteryDiagnosis]

What these people are not saying, and perhaps what they don't know, is that a group of sugar/protein "whiskers" that sit on the cell surface of immune cells referred to as cluster determinant 95 or CD95 are virtually non-existant in persons who suffer with Lupus. What they don't study are the effects of natural substances on the body's ability to better form and produce these sugar/protein "whiskers". (Glycoproteins)

What they would benefit from knowing is that CD95 is responsible for letting an immune cell "know" that it has turned on the body, and that it needs to DIE. (apoptosis) This is a normal process, that is obviosly not normal in persons who suffer with autoimmune conditions. A potential reason for this "autoimmunity" is that they are NOT PRODUCING ENOUGH HIGHLY SPECIFIC SUGARS to properly/sufficiently construct glycoproteins, in particular CD95.

http://www.arthritis.org/research/ResearchUpdate/03Sept...

Death for T and B cells
The immune system is normally tightly controlled so that it is only deployed in response to foreign invaders. But sometimes, the system breaks down and mistakenly attacks the body’s own cells and organs. For instance, some immune cells called T cells attack the joint lining in rheumatoid arthritis (RA), while B cells create damaging proteins that are common in lupus. Scientists are making significant progress in determining how best to seek out and destroy just these harmful immune cells while leaving other parts of the body’s disease fighting system intact.

And the evidence that apoptosis is deficient in persons who suffer with Lupus....


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retri...
Rom J Intern Med. 2000-2001;38-39:83-8. Related Articles, Links

Serological levels of apoptotic bodies, sFAS and TNF in lupus erythematosus.

Alecu M, Coman G, Alecu S.

Dermatological Reaseach Center, Scarlat Longhin Hospital for Dermatology, 216, Sos. Serban Voda, 73202, Bucharest, Romania.

In our study we have investigated the presence of apoptotic bodies, soluble FAS receptor and TNF (tumor necrosis factor) in three clinical forms of lupus erythematosus. Determinations were performed in attack period of: systemic lupus erythematosus (SLE) for 20 patients, 20 patients with subacute cutaneous lupus erythematosus (SCLE), 20 patients with chronic discoid lupus erythematosus (DLE). Determinations were performed by ELISA (for apoptotic bodies, kit Boehringer, normal values 400-800 mU), (for sFAS, kit R&D Systems, normal values 4500-17000 pg/ml) (for TNF, ELISA kit R&D Systems, normal values 0.4-3.6 pg/ml). Results in SLE: apoptotic bodies were increased in 16 cases (980-1030); sFAS in 18 cases (17000-24000 pg/ml) TNF was increased in all 20 cases (40-140 pg/ml). In SCLE with multiple cutaneous lesions and without internal organs disturbance the apoptotic bodies were increased in 10 cases (960-1030 pg/ml), sFAS in 9 cases (17000-22000 pg/ml), and TNF alpha in 9 cases. In DLE, apoptotic bodies were increased in 2 patients (980-1010 pg/ml), sFAS in 3 patients (17000-20000 pg/ml) and TNF in 2 patients (20-40 pg/mil). Investigated values were slightly correlated with immune parameters (anti dsDNA antibodies), but they were correlated with the presence of renal disturbances or extension of cutaneous lesions. We consider that the presence of increased apoptotic bodies as a result of peripheral mononuclear cells apoptosis appear as a nauto-limiting mechanism in a pathological immune response. The increase of sFAS in lupus patients serum might be interpreted as an alteration of apoptosis respectively a deficit in apoptosis which has as a first consequence the persistence of B and T lymphocytes, activated, in the pathogen immune response.

PMID: 15529575