Inflammation cell types induced

Sato N, Ahuja SK, Quinones M, et al. CC chemokine receptor (CCR)2 is required for langerhans cell migration and localization of T helper cell type 1 (Thl)-inducing dendritic cells. Absence of CCR2 shifts the Leishmania major-resistant phenotype to a susceptible state dominated by Th2 cytokines, b cell outgrowth, and sustained neutrophilic inflammation. J Exp Med 2000 192(2) 205-218. 

IL-13 on keratinocytes, two Th-2 cytokines which function via the same receptor in this cell type [26]. IL-13 or IL-4-stimulated keratinocytes attract CCR4+CD4-I- Th-2 cells via CCL22 [27]. Moreover, IL-13 induces the expression of MMP-9 in keratinocytes [28] which may play a crucial role in atopic skin inflammation by facilitating the migration of leukocytes into the epidermis. 

Hypophysectomy leads to an 80% decrease in interstitial fluid volume which is returned to normal by injection of hCG. The mediator of this effect is either produced directly by the Leydig cells in response to LH or originates in other cell types, e.g., macrophages or Sertoli cells in response to Leydig cell factors. The increases in interstitial fluid volume may be caused by mechanisms similar to those inducing oedema in acute inflammation. After hCG treatment, polymorphonuclear leukocytes (PMNs) accumulate in testicular blood vessels prior to the increases in the interstitial fluid volume and then migrate into the interstitial spaces 4 and 8 h after injection this invasion by PMNs may be caused by the release of a chemotactic agent [97]. 

The eukaryotic transcription factor NF-kB was identified as a protein that binds specifically to a decameric DNA sequence (ggg ACT TTC C), within the intronic enhancer of the immunoglobulin kappa light chain in mature B and plasma cells, but not pre-B cells [32, 33]. This transcription factor consists of homo- or heterodimers of different subunits which are members of a family of structurally related proteins (Rel/NF-icB proteins). NF-kB has been detected in most cell types, and specific NF-kB binding sites have been identified in promoters and enhancers of numerous inducible genes. Thus, it has been shown that NF-kB plays a pivotal role in the coordinated transactivation of many genes involved in cytokine-mediated inflammation. 

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