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)

Human thyroid cells are resistant to lysis by the homologous membrane attack complex. By immunohistochemical staining we here show that normal thyroid cells and those in Graves' disease and Hashimoto's thyroiditis express two membrane attack complex-inhibiting proteins, CD59 antigen and membrane attack complex-inhibiting protein/homologous restriction factor (MIP/HRF). In vitro, the expression of both molecules was enhanced by interleukin-1 (IL-1), tumour necrosis factor (TNF) and interferon-gamma (IFN-gamma) and cytokine-treated thyroid cells were more resistant to lysis by homologous complement. Blocking experiments with monoclonal antibodies against CD59 antigen and MIP/HRF showed that both molecules contributed but CD59 antigen was the more important in mediating resistance to complement attack. Expression of these proteins may be an important determinant of the severity of tissue injury produced by complement-fixing thyroid peroxidase antibodies in autoimmune thyroid disease.
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PMID:Expression and function of membrane attack complex inhibitory proteins on thyroid follicular cells. 137 92

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

IL-17A is a critical, proinflammatory cytokine essential to host defense and is induced in response to microbial invasion. It stimulates granulopoiesis, leading to neutrophilia, neutrophil activation, and mobilization. TPO synergizes with other cytokines in stimulating and expanding hematopoietic progenitors, also leading to granulopoiesis and megakaryopoiesis, and is required for thrombocytopoiesis. We investigated the effects of in vivo expression of IL-17A on granulopoiesis and megakaryopoiesis in TPO receptor c-mpl-/- mice. IL-17A expression expanded megakaryocytes by 2.5-fold in normal mice but had no such effect in c-mpl-/- mice. The megakaryocyte expansion did not result in increased peripheral platelet counts. IL-17A expression did not impact bone marrow precursors in c-mpl-/- mice; however, it expanded splenic precursors, although to a lesser extent compared with normal controls (CFU-HPP). No peripheral neutrophil expansion was observed in c-mpl-/- mice. Moreover, in c-mpl-/- mice, release of IL-17A downstream cytokines was reduced significantly (KC, MIP-2, GM-CSF). The data suggest that IL-17A requires the presence of functional TPO/c-mpl to exert its effects on granulopoiesis and megakaryopoiesis. Furthermore, IL-17A and its downstream cytokines are important regulators and synergistic factors for the physiologic function of TPO/c-mpl on hematopoiesis.
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PMID:Requirement of TPO/c-mpl for IL-17A-induced granulopoiesis and megakaryopoiesis. 2399 Jun 27