Systemic lupus erythematosus (SLE) is a chronic autoimmune connective tissue disease characterised by multivisceral involvement and the presence of autoantibodies. In this context, C‐reactive protein (CRP) holds a particular position: a moderate rise accompanies autoimmune flares, whereas a sharp elevation suggests an infection or specific inflammatory manifestations. This study aimed to analyse the factors associated with increased CRP levels in women with lupus followed at the Cocody University Hospital in Abidjan. This was a cross‐sectional observational study including 62 adult women with SLE (ACR/EULAR criteria). Collected variables included socio‐demographic, clinical, biological and immunological data. CRP was categorised into three groups: (<6 mg/L, 6–20 mg/L and >20 mg/L). Univariate and multivariate analyses were performed using binary logistic regression, supplemented by the estimation of marginal effects. The results show a mean CRP concentration of 28.2 ± 21.2 mg/L. A CRP level >20 mg/L was common and significantly associated with renal manifestations, arthralgia/arthritis and the severity level of pain. Biologically, proteinuria ≥0.5 g/24 h, hypercreatininemia and leukocytosis were strongly correlated with elevated CRP. In multivariate regression, only hypercreatininemia remained significant (odds ratio [OR] = 24.8; p = 0.011). The estimation of marginal effects confirmed its major impact (+47.5 probability points), as well as that of proteinuria (+31.3 points) and obesity (+14.1 points), while overweight appeared protective (−19.2 points). The SLE Disease Activity Index (SLEDAI) score was positively but modestly correlated with CRP (+1.4 probability points/unit). The model’s ROC curve showed excellent performance (area under the ROC curve [AUC] = 0.84). In conclusion, elevated CRP levels were primarily associated with renal manifestations, notably proteinuria and elevated serum creatinine, as well as with disease activity. CRP could therefore serve as a complementary biomarker in the assessment of patients with SLE, particularly in the presence of renal involvement. However, these results should be interpreted as associations and require confirmation by longitudinal studies.
The intestine is the largest peripheral lymphoid organ in humans and interacts with a vast intestinal microbiota. There is a growing awareness that the intestinal microbiota plays a crucial role in training, functioning, and inducing the host immune system, affecting the overall health of the host. However, the composition of the intestinal microbiota varies with factors such as ethnicity, geographical location, and diet, making it difficult to form a universal pattern. Microbial metabolites are regarded as messengers of the intestinal microbiota, capable of generating unique molecules that humans cannot produce. Many cells of the immune system also express receptors for these molecules, playing a key role in guiding the differentiation of immune cells. Short-chain fatty acids (SCFAs) produced through the fermentation of dietary fiber, particularly butyrate, serve as key mediators linking gut microbial metabolism to host immune regulation. Accumulating evidence indicates that butyrate contributes to the maintenance of immune homeostasis by modulating immune cell metabolism, differentiation, cytokine production, and intercellular communication. The immunological effects of butyrate cannot be simply categorized as immunosuppressive or tolerance-inducing. Instead, its functional outcomes are shaped by multiple factors, including immune cell type, local concentration, tissue microenvironment, route of administration, and disease context. This context-dependent nature highlights the complexity of butyrate-mediated immune regulation and underscores the need for a more comprehensive understanding of its mechanisms of action. This review summarizes the effects of butyrate on macrophages, dendritic cells (DCs), lymphocytes, and neutrophils with respect to cellular metabolism, differentiation, cytokine secretion, and intercellular communication. In addition, common underlying mechanisms, including histone deacetylase (HDAC) inhibition, metabolic reprogramming, and G protein–coupled receptor (GPCR) signaling, together with current controversies and knowledge gaps, are discussed to provide new insights into the role of butyrate in maintaining immune homeostasis.
MICA (major histocompatibility complex class I [MHC class I] chain‐related protein A) is a stress‐induced glycoprotein that functions as a ligand for the NKG2D (natural killer [NK] group 2 member D) receptor, expressed on NK cells and CD8 + T lymphocytes (cytotoxic T cells), playing a key role in tumor immune surveillance. In melanoma, modulation of this axis promotes tumor immune evasion. The functional MICA‐129 polymorphism (methionine [Met]/valine [Val]) alters the binding affinity to NKG2D, thereby influencing the cytotoxic immune response. This study included patients with basal cell carcinoma (BCC) and melanoma (primary and metastatic). The Functional Assessment of Cancer Therapy–Melanoma (FACT‐M) questionnaire was administered, followed by MICA‐129 genotyping using quantitative polymerase chain reaction (qPCR), measurement of soluble MICA (sMICA) by enzyme‐linked immunosorbent assay (ELISA), analysis of MICA and NKG2D expression on CD8 + T lymphocytes by flow cytometry, and assessment of inflammatory cytokines and angiogenic factors. A higher frequency of the Val/Val genotype was observed in metastatic melanoma, whereas serum sMICA levels did not differ among the groups. The Val variant was associated with reduced functional stability of the MICA–NKG2D axis, favoring tumor immune evasion. Primary melanoma exhibited a more pronounced inflammatory profile, whereas metastatic melanoma showed greater angiogenic activity, indicating a microenvironment conducive to tumor progression. These findings suggest that the MICA‐129 Val/Val genotype may serve as a prognostic biomarker and support the MICA–NKG2D axis as a potential therapeutic target in melanoma.
Pregnancy requires balanced maternal immune regulation for healthy fetal development, in which γδT cells contribute at the feto-maternal interface; however, mechanisms guiding decidual γδT-cell accumulation remain unclear. We analyzed chemokine receptor (ChR) expression (C-C motif ChR [CCR]5, CCR6, and C-X-C motif ChR [CXCR]4) and cytokine profiles of peripheral γδT cells from first-trimester pregnant and nonpregnant women by multicolor flow cytometry under baseline and antigen-independent activation, while cytokine modulation was assessed in isolated γδT cells co-cultured with trophoblasts using cytometric bead array (CBA). While the frequency of ChR-expressing γδTCR+ cells was largely preserved, CCR6 and CXCR4 expression intensities were slightly elevated during pregnancy. Although single ChR expression did not differ between conventional and natural killer (NK)-like γδT cell subsets, the proportions of some ChR co-expressing populations were slightly but significantly higher among NK-like γδT cells. Within the observed co-expression patterns, CCR5/CCR6 was the most frequent combination on γδT cell subsets. Furthermore, different stimulation models differently shaped ChR expression on conventional γδT cells, with physiological activation maintaining CCR5+ dominance alongside elevated CXCR4+ cell ratios, whereas PMA/Ionomycin stimulation was characterized by a predominance of CXCR4+ cells and a low proportion of CCR5+ cells. In terms of cytokine production γδT cells exhibited a broad Th1-like cytokine profile dominated by IL-2, TNF-α, and IFN-γ, with modest reductions in TNF-α and IFN-γ during pregnancy. Trophoblast contact further attenuated this response by inhibiting IL-2, TNF-α, and IL-17A release, while markedly enhancing IL-6 production. Our findings suggest that γδT cell subsets slightly differ in ChR co-expression patterns, and ChRs are differentially regulated by distinct activation processes. The modest differences observed during first-trimester pregnancy indicate a conserved migratory capacity, with pregnancy-specific migratory phenotypes likely shaped at the materno-fetal interface. Additionally, γδT cells exhibited an inflammatory cytokine milieu that was modulated upon trophoblast contact, which may contribute to trophoblast-mediated immune adaptations during human pregnancy.
B cells are key contributors to the immunopathogenesis of rheumatoid arthritis (RA), yet the expression profile of interleukin-17 (IL-17) receptors on human B cells remains incompletely defined. We analyzed the surface expression of IL-17RA–IL-17RE on peripheral CD19+ B cells from 42 patients with RA and 20 healthy controls (HC) using flow cytometry. Receptor-positive cell frequency and mean fluorescence intensity (MFI) were evaluated, and disease activity was assessed using the Disease Activity Score in 28 joints based on erythrocyte sedimentation rate (DAS28-ESR). The frequency of receptor-positive B cells differed significantly among IL-17 receptor (IL-17R) family members in both RA and HC, with IL-17RD showing the highest proportion of positive cells, followed by IL-17RA, whereas IL-17RC was less frequent and IL-17RB and IL-17RE were rarely detected. The proportion of IL-17RA+ B cells was lower in RA than in HC and remained statistically significant after correction for multiple comparisons (Holm-adjusted p=0.0126). A nominally lower frequency of IL-17RC+ B cells in RA did not remain significant after adjustment, while IL-17RD frequency was comparable between groups. No between-group differences in MFI remained significant after multiple-comparison correction. Receptor expression was not significantly associated with DAS28-ESR disease activity categories. These findings provide a descriptive characterization of the IL-17R family on peripheral B cells in RA and identify a lower frequency of IL-17RA+ B cells as the most robust between-group difference, suggesting alterations in IL-17R dynamics that may contribute to B-cell dysregulation and disease pathogenesis.
