Epigenetic and metabolic regulation of macrophage responsiveness and memory

J Immunol. 2025 Jul 1:vkaf135. doi: 10.1093/jimmun/vkaf135. Online ahead of print. ABSTRACT Macrophages, the central mediators of innate immune responses, can adapt and build nonspecific memory, also known as innate immune memory or trained immunity. Training of macrophages occurs through epigenetic changes and metabolic rewiring, which fuels macrophage responsiveness. In addition to training in response … Read more

HMGB1 inhibits the IFN-γ-induced PD-L1 expression in NSCLC

J Immunol. 2025 Jun 28:vkaf125. doi: 10.1093/jimmun/vkaf125. Online ahead of print. ABSTRACT T cells are the most important cytotoxic cells involved in antitumor immune responses. After recognizing the major histocompatibility complex (MHC)-peptide complex, cytokines including interferon-γ (IFN-γ) are released to kill tumor cells. However, IFN-γ can also induce tumor cells to express PD-L1. This molecule … Read more

Transcription factor Rel regulates the transcription of effector genes involved in immune response by cooperating with IκBs in lamprey (Lethenteron reissneri)

J Immunol. 2025 Mar 1;214(3):472-488. doi: 10.1093/jimmun/vkae060. ABSTRACT The Rels, a class of nuclear factor κB (NF-κB) complexes, regulate diverse physiological processes by modulating the transcription of effector genes. IκBs are the critical proteins that inhibit NF-κB nuclear translocation, thereby disrupting NF-κB-mediated signaling pathways. Despite this, the precise role and underlying molecular mechanisms of Rel … Read more

Distinct expression of CD56 and CD19 marks molecular and functional endotypes of tetanus- versus RBD-specific human bone marrow plasma cells

J Immunol. 2025 Jun 24:vkaf059. doi: 10.1093/jimmun/vkaf059. Online ahead of print. ABSTRACT Plasma cell survival is influenced by various factors, including soluble mediators, intrinsic and extrinsic signals as well as adhesion molecules defining the bone marrow microenvironment. The role of their induction, turnover and competition dynamics among different antigen-specific bone marrow plasma cell subsets is … Read more

MHC II-restricted presentation of soluble antigen by naïve B cells is impaired upon engagement with membrane-associated antigen: A potential mechanism to mitigate autoreactivity

J Immunol. 2025 Jun 23:vkaf129. doi: 10.1093/jimmun/vkaf129. Online ahead of print. ABSTRACT T cell tolerance to self can prevent self-reactive B cells from mounting effective autoimmune responses by limiting their available help. However, tolerance may be compromised during infection if small amounts of soluble cross-reactive pathogen antigens containing functional T cell epitopes are released for … Read more

G9a controls plasma cell differentiation through FOXO1 and ETS1 binding site regulatory networks

J Immunol. 2025 Jun 23:vkaf127. doi: 10.1093/jimmun/vkaf127. Online ahead of print. ABSTRACT B cell differentiation is tightly regulated through coordinated changes in metabolism, division, expression of transcription factors, and epigenetic programming mediated by histone modifying enzymes. Here, we examined the role of an epigenetic writer, the histone H3K9 mono and dimethyltransferase G9a, in B cell … Read more

Cytokine and metabolite networks shape T cell residency and functionality at the term human maternal-fetal interface

J Immunol. 2025 Jun 23:vkaf093. doi: 10.1093/jimmun/vkaf093. Online ahead of print. ABSTRACT Placentation presents immune conflict between mother and fetus, yet in normal pregnancy maternal immunity against infection is maintained without expense to fetal tolerance. This is believed to result from adaptations at the maternal-fetal interface (MFI), which affect T cell programming, but the identities … Read more

Isolation of mitochondrial mutation-specific T cell receptors

J Immunol. 2025 Jun 30:vkaf139. doi: 10.1093/jimmun/vkaf139. Online ahead of print. ABSTRACT Neoantigen-specific T cells play a major role in cancer immunotherapy. Mutated proteins derived from non-synonymous mutations in tumor genomic DNA are the major source of neoantigens. It is conceivable that non-synonymous mutations found in tumor mitochondrial DNA (mtDNA) can also generate neoantigens that … Read more

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