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《Immunobiology》2022,227(3):152193
Uncontrolled inflammation is the underlining mechanism of many human diseases and the increasing prevalence of such diseases mandate to develop new anti-inflammatory treatments. Utilizing the anti-inflammatory properties as well as other protective/beneficial features of natural IgMs (nIgMs) for treatment of human disorders seems as an easily accessible goal by the use of blood-purified IgMs as an alternative for polyclonal nIgMs. Despite the other blood cells, the functions of platelets have not been inspected under the influence of blood IgMs adequately. However, platelets, the second most numerous blood cells, are involved in the pathology of many inflammatory disorders through the production/expression of many inflammatory molecules.Thus, in the present study, we purified IgMs from serum of healthy donors and plasma of patients with systemic lupus erythematosus (SLE). Subsequently, we carried out comparative analysis of the inflammatory functions of normal platelets (P-selectin expression, GPIIb/IIIa activation, and secretion of soluble CD40L and TNF-α) that were stimulated by SLE microparticles (as key endogenous inflammation-drivers) in the presence or absence of the two IgM preparations; one with normal level of nIgMs (healthy blood IgMs) and the other with likely altered nIgM content (SLE blood IgMs). Both blood IgM preparations could suppress the elevated activation parameters of platelets in response to SLE microparticles. Additionally, the impact of SLE blood IgMs on the platelets was not superior to that of normal blood IgMs.The anti-inflammatory effects of blood IgMs on the activated platelets have been shown for the first time in the present study. Thus, this study provides evidence in favor of use of healthy blood IgMs as an anti-inflammatory therapy in clinical settings. 相似文献
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Lens thickness and associated factors in Chinese children: The Shandong Children Eye Study
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《Cancer cell》2022,40(3):277-288.e3
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《Immunobiology》2022,227(5):152256
Excessive activation of Toll-like receptor (TLR) leads to sepsis. Inflammatory responses to various microbiological components are initiated via different TLR proteins, but all TLR signals are transmitted by TRAF6. We reported that TRAF6 associated with ubiquitinated IRAK-1 undergoes proteasome-mediated degradation, suggesting that IRAK-1 has a negative regulatory role in TLR signaling. Here, we investigated the minimal structural region of IRAK-1 needed for degradation of TRAF6. The IRAK-1 protein contains an N-terminal death domain (DD; amino acids 1–102), a serine/proline/threonine-rich ProST domain (amino acids 103–197), a central kinase domain with an activation loop (amino acids 198–522), and the C-terminal C1 and C2 domains (amino acids 523–712), which contain two and one putative TRAF6-binding (TB) sites, respectively. TRAF6 degradation was severely impaired by deletion of the DD or C1 domain, and a mutant (DC1) containing only the DD and C1 domains could induce TRAF6 degradation. IRAK-1 mutants lacking the N- or C-terminal amino acids of DD induced little degradation. Deletion or mutation of TB2 (amino acids 585–591) in the C1 domain also inhibited TRAF6 degradation. An IRAK-1 mutant possessing only DD and TB2 did not induce TRAF6 degradation, although a mutant in which a short spacer was inserted between DD and TB2 induced TRAF6 degradation, which and DC1-induced degradation were inhibited by proteasome inhibitors. All IRAK-1 mutants that induced TRAF6 degradation could be immunoprecipitated with TRAF6. Meanwhile, NF-κB activation was observed for all IRAK-1 mutants–including those that failed to induce degradation and was severely impaired only for a mutant carrying mutations in both TBs of C1. These results demonstrate that only DD and TB2 separated by an appropriate distance can induce TRAF6 degradation. Conformational analysis of this minimal structural unit may aid development of low molecular compounds that negatively regulate TLR signaling. 相似文献
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