Immunologic Approaches to the Therapy of Autoimmune Salivary Gland Disease

1987 ◽  
Vol 66 (2_suppl) ◽  
pp. 703-708
Author(s):  
H.C. Lane ◽  
A.S. Fauci

A variety of immunologic mechanisms may theoretically give rise to disease in the salivary glands. Among them are abnormal antibody production, hyper-reactive T-lymphocytes, and mono- or oligoclonal expansions of B-lymphocytes, While it is not clear which, if any, of these mechanisms are of prime importance in the immunopathology of salivary gland disease, they provide a framework, within which to discuss theoretical approaches to the treatment of autoimmune salivary gland disease. Among the techniques used to decrease antibody-induced damage are non-steroidal anti-inflammatory agents, plasmapheresis, and corticosteroids. Cyclosporin, monoclonal antibodies, and biologic response-modifiers may be used to modulate T-cell function, and anti-idiotype antibodies or immunosuppressive agents may be used to treat malignant expansions of B-cells. Although the generally benign nature of autoimmune salivary gland disease precludes the use of many of the potentially toxic treatment regimens discussed here, the appreciation of these approaches to immunomodulation provides a basis upon which to develop new and innovative therapeutic strategies.

1987 ◽  
Vol 66 (1_suppl) ◽  
pp. 703-708
Author(s):  
H.C. Lane ◽  
A.S. Fauci

A variety of immunologic mechanisms may theoretically give rise to disease in the salivary glands. Among them are abnormal antibody production, hyper-reactive T-lymphocytes, and mono- or oligoclonal expansions of B-lymphocytes, While it is not clear which, if any, of these mechanisms are of prime importance in the immunopathology of salivary gland disease, they provide a framework, within which to discuss theoretical approaches to the treatment of auto-immune salivary gland disease. Among the techniques used to decrease antibody-induced damage are non-steroidal anti-inflammatory agents, plasmapheresis, and corticosteroids. Cyclosporin, monoclonal antibodies, and biologic response-modifiers may be used to modulate T-cell function, and anti-idiotype antibodies or immunosuppressive agents may be used to treat malignant expansions of B-cells. Although the generally benign nature of auto-immune salivary gland disease precludes the use of many of the potentially toxic treatment regimens discussed here, the appreciation of these approaches to immunomodulation provides a basis upon which to develop new and innovative therapeutic strategies.


Author(s):  
B Hofauer ◽  
N Mansour ◽  
M Bas ◽  
K Stock ◽  
A Knopf

1984 ◽  
Vol 20 (4) ◽  
pp. 795 ◽  
Author(s):  
E Y Kang ◽  
S J Cha ◽  
S H Cha ◽  
H Y Seol ◽  
K B Chung ◽  
...  

1982 ◽  
Vol 156 (2) ◽  
pp. 658-663 ◽  
Author(s):  
G Nabel ◽  
W J Allard ◽  
H Cantor

We previously described a cloned cell line that combines information for a unique display of cell surface antigens and specialized function similar to activated natural killer (NK) cells. In addition to conventional cellular targets such as the YAC-1 and MBL-2 lymphomas, this cloned line also lysed lipopolysaccharide-activated B lymphocytes. To determine whether some NK cells can inhibit B cell function, we tested the ability of NK-like clones to suppress Ig secretion in vitro and in vivo. These cloned cells suppressed Ig secretion when they constituted as few as 0.2% of the total cell population and inhibition did not require identity at the H-2 locus. We suggest that some NK cells might recognize non-major histocompatibility complex gene products on activated B lymphocytes and lyse these cells, and this might represent a fundamental cell-cell interaction that regulates antibody secretion by activated B cells.


1975 ◽  
Vol 142 (5) ◽  
pp. 1306-1311 ◽  
Author(s):  
B R Bloom ◽  
E Shevach

The question whether B lymphocytes are capable of being activated by antigen in the absence of functional T cells was investigated in a model that excludes participation of T cells by virtue of an immune response gene restriction. Strain 2 guinea pigs are capable of responding to immunization with DNP-PLL, whereas strain 13 animals are not. In the present experiments, animals of both strains were immunized with DNP-PLL complexed to ovalbumin (DNP-PLL-Ova) under conditions in which equal titers of antibodies to DNP were produced by both strains. The failure of T cells of strain 13 animals to respond to DNP-PLL was confirmed by the virus plaque assay. While spleen cells from both strains produced MIF after stimulation with DNP-PLL-Ova, in response to DNP-PLL only strain 2 spleens were able to produce MIF. Cells from neither strain could be activated by DNP-guinea pig albumin to produce MIF. We conclude that B lymphocytes are incapable of being stimulated by antigen in the absence of T cells, and that MIF production is a thymus-dependent response. While the results indicate that MIF production is a valid qualitative assay for T-cell competence, since MIF can be produced by B and T cells, the degree of migration inhibition cannot be regarded as a quantitative measure of T-cell function.


1997 ◽  
Vol 35 (3) ◽  
pp. 218
Author(s):  
A. Schmidt-Westhausen ◽  
H.D. Pohle ◽  
H. Lobeck ◽  
P.A. Reichart

Rheumatology ◽  
2020 ◽  
Vol 59 (Supplement_3) ◽  
pp. iii74-iii78 ◽  
Author(s):  
Rona Smith

Abstract The introduction of immunosuppressive therapies has transformed ANCA-associated vasculitis (AAV) from a largely fatal condition to a chronic relapsing disorder. However, progressive organ damage and disability, both from the disease process itself and from therapies used for treatment, eventually affect the majority of patients. Infection, rather than uncontrolled vasculitis, is the greatest cause of early mortality and remains a major problem thereafter. Increased rates of malignancy and cardiovascular disease are additional important long term sequelae. This review focuses on the complications associated with the immunosuppressive therapies most commonly used to treat ANCA-associated vasculitis, and considers prophylactic and monitoring strategies to minimize these risks. Achieving a balance between immunosuppression to reduce relapse risk and minimizing the adverse effects associated with therapy has become key. The contribution of glucocorticoids to treatment toxicity is increasingly being recognized, and future therapeutic strategies must concentrate on glucocorticoid minimization or sparing strategies. Development of robust predictors of an individual’s future clinical course is needed in order to individually tailor treatment regimens.


2014 ◽  
Vol 25 (2) ◽  
pp. 142-149
Author(s):  
Yoon-Ju Lee ◽  
Sung-Chan Shin ◽  
Won-Jae Cha ◽  
Byung-Joo Lee ◽  
Soo-Geun Wang

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