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The molecular mechanisms by which CaMs may regulate disease resistance are unknown.
Several studies have reported that TLR4 and TLR9 may regulate disease severity of EAE, but the detailed functions of TLRs during MS/EAE are still controversial (Kerfoot et al, 2004; Marta et al, 2008; Prinz et al, 2006).
These observations led to the speculation that DNase I may regulate disease progression by degrading DNA released from dying cells, thereby reducing the antigen load driving the immune response, and by facilitating the hydrolysis of circulating and/or deposited DNA-antibody complexes [ 26].
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Therefore, one may suggest that collagen fibrils retain crypto-biological features [62] that may intrinsically regulate disease progression and physiological events involving MMP degradation.
Furthermore, we have also uncovered novel microRNA-gene interactions that may regulate the disease progression from latent to active TB.
Nevertheless, as TNFAIP6 is upregulated in response to TNF-α, there is a possibility that TNFAIP6 may regulate the disease progression of BLV-induced leukemogenesis.
These facts prompted us to investigate the possibility that Sema3A expression and/or the balance of Sema3A and VEGF165 expression may regulate the disease activity of RA including inflammation, angiogenesis and proliferation of synovial cells.
Finally, our results suggest that SlCaM2 and SlCaM6 may employ different molecular mechanisms to regulate disease resistance.
Discovered markers may also define a subset of networked causal genes that regulate disease phenotype.
Furthermore, recent evidence suggests that muscle fiber recruitment during LIPA may potentially produce cellular signals which may regulate risk factors for disease [ 20].
In this review, we have summarized the sources of RANKL in periodontal disease and explored which factor may regulate RANKL expression in this disease.
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