Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.59 (MIP)
 4,906 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemokines are a large family of cytokines, which may be involved in the pathogenesis of a wide variety of inflammatory or autoimmune conditions. The role of chemokines in chronic autoimmune thyroiditis is unknown. We sought to examine the role of CC chemokines in chronic autoimmune thyroiditis. We measured serum levels of CC chemokines, including monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein 1a and 1b (MIP-1a and MIP-1b) in 32 women with chronic autoimmune thyroiditis in comparison with 2 control groups (33 apparently healthy women and 43 women with benign cold thyroid nodules) by enzyme-linked immunosorbent assay (ELISA). We found a 45% increase in serum MCP-1 levels in women with chronic autoimmune thyroiditis compared with either of the 2 control groups (P =.01). There was no difference in either serum MIP-1a (P =.69) or MIP-1b (P =.81) levels between women with chronic autoimmune thyroiditis and controls. Among women with chronic autoimmune thyroiditis, women with a family history of hypothyroidism had a 59% increase in serum MCP-1 levels compared with women with no family history of hypothyroidism (P =.02). Serum MCP-1 levels were associated with serum levels of antithyroid peroxidase (r =.2, P =.03) (anti-TPO Ab) and antithyroglobulin (r =.2, P =.04) antibodies (anti-TG Ab). There was no association between serum MCP-1 levels and serum free thyroxine index (P =.57), triiodothyronine (T(3)) (P =.47) or thyroid-stimulating hormone (TSH) (P =.47) levels. Serum MCP-1 is increased in women with chronic autoimmune thyroiditis, especially in the presence of a family history of hypothyroidism, indicating a possible pathogenetic role for MCP-1 in this condition.
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PMID:Serum monocyte chemoattractant protein-1 is increased in chronic autoimmune thyroiditis. 1240 3

Although adjuvants are essential for the initiation of experimental autoimmune diseases, their precise contribution to the pathological manifestations is still poorly understood. Experimental autoimmune thyroiditis (EAT) is interesting in that respect because it can be initiated with the help of two different adjuvants Freund's complete or LPS which may initiate independent pathogenic pathways. In the present study, we have compared Freund's-induced versus LPS-induced EAT with respect to their dependence upon CD8+ T cells, which are considered as major actors in the pathogenesis of thyroiditis. Our results reveal that whereas CD8+ T cells are mandatory in the Freund's model, they can be bypassed in the LPS model. On the basis of this finding, we have examined the possibility that LPS may act directly upon in vitro cultured thyrocytes with no intermediate cell stages. Indeed, LPS triggers transcription and protein synthesis of several chemokines such as MIP-3alpha, RANTES, MCP-1 or TARC. Thus, beside enhancing the immunogenicity of autoantigens, probably via antigen trafficking and presentation, adjuvants such as LPS directly interact with the target organ through synthesis and release of powerful T cell attractants that facilitate its lymphocytic infiltration.
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PMID:LPS and Freund's adjuvant initiate different inflammatory circuits in experimental autoimmune thyroiditis. 1279 14