Targeting Macrophage Polarization in Infectious Diseases: M1/M2 Functional Profiles, Immune Signaling and Microbial Virulence Factors.

IF 2.9 4区 医学 Q3 IMMUNOLOGY Immunological Investigations Pub Date : 2024-10-01 Epub Date: 2024-06-24 DOI:10.1080/08820139.2024.2367682
Cláudio Daniel Cerdeira, Maísa R P L Brigagão
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Abstract

Introduction: An event of increasing interest during host-pathogen interactions is the polarization of patrolling/naive monocytes (MOs) into macrophage subsets (MФs). Therapeutic strategies aimed at modulating this event are under investigation.

Methods: This review focuses on the mechanisms of induction/development and profile of MФs polarized toward classically proinflammatory (M1) or alternatively anti-inflammatory (M2) phenotypes in response to bacteria, fungi, parasites, and viruses.

Results and discussion: It highlights nuclear, cytoplasmic, and cell surface receptors (pattern recognition receptors/PPRs), microenvironmental mediators, and immune signaling. MФs polarize into phenotypes: M1 MФs, activated by IFN-γ, pathogen-associated molecular patterns (PAMPs, e.g. lipopolysaccharide) and membrane-bound PPRs ligands (TLRs/CLRs ligands); or M2 MФs, induced by interleukins (ILs-4, -10 and -13), antigen-antibody complexes, and helminth PAMPs. Polarization toward M1 and M2 profiles evolve in a pathogen-specific manner, with or without canonicity, and can vary widely. Ultimately, this can result in varying degrees of host protection or more severe disease outcome. On the one hand, the host is driving effective MФs polarization (M1 or M2); but on the other hand, microorganisms may skew the polarization through virulence factors to increase pathogenicity. Cellular/genomic reprogramming also ensures plasticity of M1/M2 phenotypes. Because modulation of polarization can occur at multiple points, new insights and emerging perspectives may have clinical implications during the inflammation-to-resolution transition; translated into practical applications as for therapeutic/vaccine design target to boost microbicidal response (M1, e.g. triggering oxidative burst) with specifics PAMPs/IFN-γ or promote tissue repair (M2, increasing arginase activity) via immunotherapy.

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针对传染病中的巨噬细胞极化:M1/M2 功能图谱、免疫信号转导和微生物毒力因子。
导言:在宿主与病原体相互作用的过程中,巡游/免疫单核细胞(MOs)极化为巨噬细胞亚群(MФs)的过程越来越受到关注。目前正在研究旨在调节这一过程的治疗策略:方法:这篇综述重点探讨了在细菌、真菌、寄生虫和病毒的作用下,MФs极化为经典的促炎(M1)或替代性抗炎(M2)表型的诱导/发育机制和特征:它强调了核、细胞质和细胞表面受体(模式识别受体/PPRs)、微环境介质和免疫信号转导。MФs 极化成表型:M1 MФs 由 IFN-γ、病原体相关分子模式(PAMPs,如脂多糖)和膜结合 PPRs 配体(TLRs/CLRs 配体)激活;或 M2 MФs 由白细胞介素(ILs-4、-10 和 -13)、抗原-抗体复合物和蠕虫 PAMPs 诱导。向 M1 和 M2 型的极化以病原体特异性的方式演变,有或没有强直性,差异很大。最终,这会导致不同程度的宿主保护或更严重的疾病结果。一方面,宿主正在推动有效的 MФs 极化(M1 或 M2);但另一方面,微生物可能会通过毒力因子使极化发生偏移,从而增加致病性。细胞/基因组重编程也确保了M1/M2表型的可塑性。由于极化的调节可发生在多个点上,因此新的见解和新的观点可能会在炎症到消退的转变过程中产生临床影响,并转化为实际应用,如利用特异性 PAMPs/IFN-γ 增强杀微生物反应(M1,如引发氧化爆发)或通过免疫疗法促进组织修复(M2,增加精氨酸酶活性)的治疗/疫苗设计目标。
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来源期刊
Immunological Investigations
Immunological Investigations 医学-免疫学
CiteScore
5.50
自引率
7.10%
发文量
49
审稿时长
3 months
期刊介绍: Disseminating immunological developments on a worldwide basis, Immunological Investigations encompasses all facets of fundamental and applied immunology, including immunohematology and the study of allergies. This journal provides information presented in the form of original research articles and book reviews, giving a truly in-depth examination of the latest advances in molecular and cellular immunology.
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