Abstract
Nuclear envelope lamin A/C proteins are a major component of the mammalian nuclear lamina, a dense fibrous protein meshwork located in the nuclear interior. Lamin A/C proteins regulate nuclear mechanics and structure and control cellular signaling, gene transcription, epigenetic regulation, cell cycle progression, cell differentiation, and cell migration. The immune system is composed of the innate and adaptive branches. Innate immunity is mediated by myeloid cells such as neutrophils, macrophages, and dendritic cells. These cells produce a rapid and nonspecific response through phagocytosis, cytokine production, and complement activation, as well as activating adaptive immunity. Specific adaptive immunity is activated by antigen presentation by antigen presenting cells (APCs) and the cytokine microenvironment, and is mainly mediated by the cellular functions of T cells and the production of antibodies by B cells. Unlike most cell types, immune cells regulate their lamin A/C protein expression relatively rapidly to exert their functions, with expression increasing in macrophages, reducing in neutrophils, and increasing transiently in T cells. In this review, we discuss and summarize studies that have addressed the role played by lamin A/C in the functions of innate and adaptive immune cells in the context of human inflammatory and autoimmune diseases, pathogen infections, and cancer.
Highlights
Lamin A/C contributes to nuclear mechanical stability, nuclear structure maintenance, and nuclear positioning, and mediates higher-order chromatin organization, epigenetic regulation, nuclear pore complex organization, gene transcription, nuclear envelope breakdown, and reassembly during mitosis, DNA replication, DNA damage response, cell cycle progression, cell differentiation, and cell polarization during migration [1,5,6,7]
Recent advances suggest that lamin A/C is finely regulated in immune cells, in both the level and the time window of expression
Lamin A/C is highly expressed, and the performance of their cell functions requires macrophages to increase its expression, while neutrophils decrease expression. This regulation appears to be related to the specific necessities of these cells types, with increased lamin A/C expression in macrophages potentially related to the exertion of proinflammatory functions and long lifespan, whereas lamin A/C inhibition in neutrophils facilitates migration while reducing lifespan
Summary
The immune system is composed of two major arms: innate and adaptive immunity. Innate immunity is mediated by myeloid cells, which generate a rapid and nonspecific response as a first line of defense. In line with this evidence, very few resting human and mouse T cells express lamin A/C, T cell activation by antigen recognition or another TCR-dependent stimulus triggers a transient and potent increase in lamin A/C mRNA and protein expression [16] In line with this finding, activation of peripheral blood mononuclear cells with the plant lectin concanavalin A results in a sharp increase in the percentage of lamin A/C positive cells [38], and lamin A/C expression is potentiated during phorbolester-mediated differentiation of HL-60 cells into macrophage-like cells [23]. CD103+ DCs in the gut, mesenteric lymph nodes, and Peyer’s patches can release RA to T cells undergoing activation [46], whereas CD103- DCs, located mainly in peripheral lymph nodes, do not produce RA [47]
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