Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several methods of inducing experimental allergic encephalomyelitis (EAE) in rats were examined using different (i) rat strains, (ii) combinations of encephalitogen with different adjuvants, and (iii) sites of encephalitogen inoculation. The time course and severity of the ensuing diseases were determined and methods delineated for inducing a disease with limited variability and high incidence. Omitting the mycobacterial component from the adjuvant eliminated the complication of adjuvant arthritis, which may develop after the appearance of EAE. Encephalitogenic emulsions prepared with an equal volume of frozen guinea pig spinal cord (GPSC) and hexadecane or squalene, injected into two inguinal nodes or one foot pad of Lewis rats, provided two quick and easy ways to induce EAE. Emulsions of encephalitogen with Freund's complete adjuvant or hexadecane, injected into the ear, also induced EAE but lengthened the time between the antigen inoculation and clinical symptoms which accompany the onset of EAE disease. However, injection into the ear offers an advantage over the Newbould technique (direct instillation of encaphalitogen in pre-exposed lymph nodes), since the animals can be confidently predosed with drugs which may reduce lymphoid mass. Effects of local inflammation on systemic drug metabolism are also minimized when using the ear route.
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PMID:Improvements for consistently inducing experimental allergic encephalomyelitis (EAE) in rats: I. without using mycobacterium. II. inoculating encephalitogen into the ear. 81 15

Rheumatoid arthritis is a complex disease associated with >100 risk loci, with the strongest association from the major histocompatibility complex (MHC) region. Here, we analyzed a new genetic association in the MHC class-III region (MHC-III) using adjuvant- and antigen-induced arthritis models. In addition, we used models for multiple sclerosis for comparison and dissected the MHC-III-mediated mechanisms of importance for antibody and T-cell responses to antigens. With the use of a panel of MHC-III recombinant inbred strains, we found that the 33-kb Ltab-Ncr3 haplotype in MHC-III was linked to the induction of arthritis with incomplete Freund's adjuvant, with similar effects in arthritis induced by several oil adjuvants (hexadecane, heptadecane, squalene, arlacel). Adoptive T-cell transfer experiment showed that this arthritis-protective effect operated during the priming of T cells by controlling their arthritogenicity. Interestingly, Ltab-Ncr3 did not regulate autoimmune diseases induced with tissue-specific antigens emulsified in adjuvant oils, such as collagen-induced arthritis or experimental autoimmune encephalomyelitis. No effect on antibody or T-cell response to tissue antigens in the Ltab-Ncr3 could be demonstrated. The finding that Ltab-Ncr3 is specific in regulating adjuvant-induced arthritis but not antigen-induced autoimmunity, and with unique effects on priming of autoreactive and arthritogenic T cells, provides new insight for understanding the regulation of autoimmune diseases.
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PMID:The Major Histocompatibility Complex Class III Haplotype Ltab-Ncr3 Regulates Adjuvant-Induced but Not Antigen-Induced Autoimmunity. 2831 76