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My optometrist said i possibly had sjogrens especially after i told her about my viral history and high lymphocytes. This was after telling her about my red eyes and inflammation etc and how antibiotics have helped which she said sometimes bacteria get caught in tear ducts etc so abx would help there. I think its the horse or cart thing going on my self but a quick google i found this which was interesting about ebv and lymphocytes etc.
III. WHAT CAUSES SJGREN'S SYNDROME
Salivary glands that produce saliva exist in "grape-like" clusters. There are no or few lymphocytes in the normal salivary gland but are present in Sjogren's syndrome. Lymphocytes are part of the immune system that normally protect us from infection and tumors. When they appear to attack our own tissues (as in Sjgren's syndrome, systemic lupus, or in rheumatoid arthritis), the term "autoimmunity" is used. Lymphocytes originate in the bone marrow. Two types of lymphocytes, termed "T cells" and "B cells" are responsible for mediating immune reactions. The T cells migrate from the bone marrow to the thymus (thus the term T cell) where they mature and then exit into their peripheral circulation. B cells migrate to particular regions in the lymph nodes where they mature; in birds, where this process was first studied, the site of maturation is the Bursa of Fabricius (thus the term, B cell). B cells make antibodies, while T cells regulate this production. "T-helper" cells promote antibody formation and "T-suppressor" cells inhibit the B cells. Other T cells can directly kill viral-infected and cancer-transformed cells (the so-called T-cytotoxic cells). The entire lymphoid system is precisely regulated, largely by messenger molecules that instruct cells to "turn on" or "turn off." Autoimmunity, the excessive reaction against one's own tissues, then results from a failure of the normal regulation of T cells and B cells. This may be due either to an excessive production of helper signals or a failure to respond to suppressor signals. As a consequence, lymphocytes infiltrate the tissues and attack normal cellular structures.
The initial trigger that sets off the autoimmune events remains unknown. Circumstantial evidence suggests that a virus is involved. One possible candidate is the Epstein-Barr virus (EBV), which causes infectious mononucleosis, a condition characterized by swollen salivary glands, joint aches and fatigue. Virtually all adults have been infected with EBV by age 20 years. After the initial infection, this virus normally resides in the salivary glands for life but causes no problems. We and others have speculated that this virus (or a closely-related virus) may trigger an autoimmune response in genetically susceptible individuals. It needs to be emphasized that there is no direct proof that EBV plays a significant role in Sjgren's syndrome. This is simply one hypothesis and experiments are currently in progress to determine its potential role. Also, Sjgren's syndrome is different from the "chronic fatigue syndrome" or the "chronic EBV syndrome." Patients with Sjgren's syndrome have characteristic abnormalities in the blood tests and salivary gland biopsies that are absent in other syndromes.
It is thought that an as yet unknown infectious agent damages the salivary gland and attracts the "immune" lymphocytes into the salivary gland. These lymphocytes release specific autoantibodies such as rheumatoid factor (RF) and antinuclear antibodies; antibodies are directed against proteins termed Sjgren's-associated antigens A and B (or SS-A and SS-B). These antibodies can enter the bloodstream and are measured in the blood tests that we obtain to confirm the diagnosis of Sjgren's syndrome. Additional T cells enter the gland and the damage is perpetuated. Under normal circumstances, a class of cells called "suppressor cells" turn off the inflammatory process. The continued destruction of the gland represents the abnormal balance of excessive action of T-helper cells and deficient action of T-suppressor cells.
There has been a great deal of research to determine hereditary factors associated with Sjgren's syndrome. To summarize these complicated studies, hereditary factors are important. Particular genes (such as human leukocyte antigen or HLA genes) are inherited in the same manner from parents as are genes for hair color or eye color; that is, one gene from each parent. The HLA genes are important in controlling the immune response and many current research studies are trying to determine exactly how they perform this task. A specific gene named HLA-DR3 is found in high frequency in Caucasian patients with primary Sjgren's syndrome. In different ethnic backgrounds, different HLA genes are associated with Sjgren's. In addition to HLA, at least four other genes are involved. Although the relative frequency of Sjgren's or lupus is slightly increased in family members of Sjgren's syndrome patients, the specific risk that children or siblings will get these diseases remains very low (<10%). In addition to genetic factors, environmental factors also play a role. It has been proposed that viral infection represents the "other factor," and that Sjgren's syndrome disease results when a genetically susceptible individual (possessing HLA-DR3) is exposed to a certain virus or viruses.
This is the link i got it from http://www.myalgia.com/sjogrens.htm
cheers!!!
III. WHAT CAUSES SJGREN'S SYNDROME
Salivary glands that produce saliva exist in "grape-like" clusters. There are no or few lymphocytes in the normal salivary gland but are present in Sjogren's syndrome. Lymphocytes are part of the immune system that normally protect us from infection and tumors. When they appear to attack our own tissues (as in Sjgren's syndrome, systemic lupus, or in rheumatoid arthritis), the term "autoimmunity" is used. Lymphocytes originate in the bone marrow. Two types of lymphocytes, termed "T cells" and "B cells" are responsible for mediating immune reactions. The T cells migrate from the bone marrow to the thymus (thus the term T cell) where they mature and then exit into their peripheral circulation. B cells migrate to particular regions in the lymph nodes where they mature; in birds, where this process was first studied, the site of maturation is the Bursa of Fabricius (thus the term, B cell). B cells make antibodies, while T cells regulate this production. "T-helper" cells promote antibody formation and "T-suppressor" cells inhibit the B cells. Other T cells can directly kill viral-infected and cancer-transformed cells (the so-called T-cytotoxic cells). The entire lymphoid system is precisely regulated, largely by messenger molecules that instruct cells to "turn on" or "turn off." Autoimmunity, the excessive reaction against one's own tissues, then results from a failure of the normal regulation of T cells and B cells. This may be due either to an excessive production of helper signals or a failure to respond to suppressor signals. As a consequence, lymphocytes infiltrate the tissues and attack normal cellular structures.
The initial trigger that sets off the autoimmune events remains unknown. Circumstantial evidence suggests that a virus is involved. One possible candidate is the Epstein-Barr virus (EBV), which causes infectious mononucleosis, a condition characterized by swollen salivary glands, joint aches and fatigue. Virtually all adults have been infected with EBV by age 20 years. After the initial infection, this virus normally resides in the salivary glands for life but causes no problems. We and others have speculated that this virus (or a closely-related virus) may trigger an autoimmune response in genetically susceptible individuals. It needs to be emphasized that there is no direct proof that EBV plays a significant role in Sjgren's syndrome. This is simply one hypothesis and experiments are currently in progress to determine its potential role. Also, Sjgren's syndrome is different from the "chronic fatigue syndrome" or the "chronic EBV syndrome." Patients with Sjgren's syndrome have characteristic abnormalities in the blood tests and salivary gland biopsies that are absent in other syndromes.
It is thought that an as yet unknown infectious agent damages the salivary gland and attracts the "immune" lymphocytes into the salivary gland. These lymphocytes release specific autoantibodies such as rheumatoid factor (RF) and antinuclear antibodies; antibodies are directed against proteins termed Sjgren's-associated antigens A and B (or SS-A and SS-B). These antibodies can enter the bloodstream and are measured in the blood tests that we obtain to confirm the diagnosis of Sjgren's syndrome. Additional T cells enter the gland and the damage is perpetuated. Under normal circumstances, a class of cells called "suppressor cells" turn off the inflammatory process. The continued destruction of the gland represents the abnormal balance of excessive action of T-helper cells and deficient action of T-suppressor cells.
There has been a great deal of research to determine hereditary factors associated with Sjgren's syndrome. To summarize these complicated studies, hereditary factors are important. Particular genes (such as human leukocyte antigen or HLA genes) are inherited in the same manner from parents as are genes for hair color or eye color; that is, one gene from each parent. The HLA genes are important in controlling the immune response and many current research studies are trying to determine exactly how they perform this task. A specific gene named HLA-DR3 is found in high frequency in Caucasian patients with primary Sjgren's syndrome. In different ethnic backgrounds, different HLA genes are associated with Sjgren's. In addition to HLA, at least four other genes are involved. Although the relative frequency of Sjgren's or lupus is slightly increased in family members of Sjgren's syndrome patients, the specific risk that children or siblings will get these diseases remains very low (<10%). In addition to genetic factors, environmental factors also play a role. It has been proposed that viral infection represents the "other factor," and that Sjgren's syndrome disease results when a genetically susceptible individual (possessing HLA-DR3) is exposed to a certain virus or viruses.
This is the link i got it from http://www.myalgia.com/sjogrens.htm
cheers!!!
