IFN-γ induces the secretion of CXCL9 and CXCL10 by skin cells, and the expression of CXCR3 on CD8⁺ T cells. CXCL9 and CXCL10 subsequently recruit CXCR3⁺ CD8⁺ T cells to attack melanocytes, induce cell death and ultimately cause vitiligo. Various immunological effects and therapeutic options are involved in this axis.

The transition of MASL to MASH occurs in three phases: (1) The detection of metabolic stress of hepatocytes by tissue-resident innate-like T cells. This triggers (2) the activation of myeloid cells and initiation of inflammation, followed by (3) escalation, meaning the recruitment and involvement of adaptive immune cells.

Immune cells are present in various CNS locations and contribute to neuroinflammation. The article reviews the role of endothelial cells on T-cell migration and functions, emphasizing the anatomical and molecular mechanisms involved in experimental autoimmune encephalomyelitis, and exploring the complex interplay between immune responses and CNS vasculature.

Immune cells from human peripheral blood and immune cells from murine spleen have been analyzed for their proteasome composition. All analyzed immune populations express almost solely immunoproteasome subunits and rather small proportions of standard proteasome subunits. This implicates a specialized role for the immunoproteasome in immune cells.

Upon injection, inert nano-/microparticle vaccine adjuvants are phagocytosed by macrophages, causing lysosomal damage. This initiates cytokine-based signaling, leading to neutrophil recruitment and NETosis. Neutrophil extracellular traps entrap adjuvant particles, limiting inflammation. Co-injected specific antigens, including synthetic peptides, elicit a strong immune response.

Co-cultures of CD4⁺ T cells and airway smooth muscle cells increased the proportion of CD45RA^-CD45RO⁺ Memory T cells; however, mitochondrial respiration and cytokine responses were not augmented. Co-cultured CD4⁺ T cells downregulated various effector T-cell genes without an upregulation of memory genes. These results demonstrate airway smooth muscle cells can induce a memory-like phenotype in CD4⁺ T cells but are not sufficient to complete the transition to memory cells.

IL-2 immunotherapy induces skin inflammation characterized by a shift towards type 2/type 17 immunity by specific increases in group 2 innate lymphoid cells (ILC2s) and dermal γδ T cells. While CD25⁺ Tregs inhibit this process, inflammation at least in part is induced through CD25⁺ effector cells in the skin.

Calreticulin, a ligand for the NK activating receptor, is induced on the surface of adipocytes after exposure to 4-hydrocynonenal (HNE) or short feeding with linoleic acid-rich high-fat diet (HFD). Calreticulin on adipocytes activates G1-ILCs in fat tissue, induces IFN-gamma production and modifies adipose inflammation.

Illustration of cartilage antibody-induced arthritis (CAIA). Arthritogenic antibodies bind and deposit onto the cartilage surface, thereby triggering the activation of FCGRs (mainly FCGR3), the release of cytokines and chemokines, and the infiltration of leukocytes.

In advanced melanoma, upregulation of IL4I1 in B2 cells impairs their recruitment into tumors and thwarts their ability to generate effector memory T cells, contributing to a B-cell-induced immunosuppressive microenvironment. Accordingly, IL4I1 antagonists would reinforce current immunotherapy in the fight against melanoma progression.