CCR9 x CXCR4

Objective : Classical follicular lymphoma (FL) is a heterogeneous malignancy. Early progression within 24 months (POD24) is linked to poor outcomes. However, precise risk stratification remains unclear. We aimed to explore chemokine receptor (CR) expression profiles as potential markers of disease biology and outcome in FL. Methods : We analyzed mRNA expression of CCR1–CCR10 , CXCR1 – CXCR5 , CX3CR1 , and XCR1 in 52 FL samples (13 POD24, 39 non‐POD24) using RT‐qPCR. Immunohistochemistry for CCR3, CCR7, CXCR3, CXCR4, and CXCR5 was performed. Reactive tonsils ( n = 5) served as controls. Results : Compared to controls, FL samples showed lower CCR1 , CCR6 , CCR7 , CXCR1 , CXCR5 , and CX3CR1 but higher CCR4 , CCR5 , CCR8 , and CCR9 expression. Grade 3a FL correlated with reduced CCR8 , CXCR1 , and CXCR3 , and increased CCR7 . POD24 cases had elevated CCR3 , CCR4 , CCR7, CXCR4 , and XCR1 but reduced CXCR3 . High CCR3 , CCR4 , and CCR10 levels were linked to inferior survival. Cluster analysis revealed two CR‐based subgroups; most POD24 cases clustered in the group with worse prognosis. Conclusion : These findings suggest distinct chemokine receptor expression profiles contribute to FL progression. Our data highlight several CRs as candidate prognostic markers and potential therapeutic targets in the context of POD24, warranting further investigation in larger, prospective cohorts. Trial Registration : The authors have confirmed clinical trial registration is not needed for this submission

Hypoxia has become one of the most critical factors limiting the development of aquaculture. Crucian carp ( Carassius auratus ) is widely consumed fish in China, with excellent tolerance to hypoxic environment. However, the molecular mechanisms underlying hypoxia adaptation and tolerance in crucian carp remain unclear. Compared with the control, increased T‐SOD, CAT, GSH‐Px, T‐AOC, ALT, and AST activities and MDA, TCHO, and TG contents, and decreased TP and ATP contents were observed after hypoxia stress. Based on RNA‐seq, 2479 differentially expressed (DE) mRNAs and 60 DE miRNAs were identified, and numerous DE mRNAs involved in HIF signaling pathway ( hif‐1α , epo , vegfa , and ho ), anaerobic metabolism ( hk1 / hk2 , pfk , gapdh , pk , and ldh ) and immune response ( nlrp12 , cxcr1 , cxcr4 , ccr9 , and cxcl12 ) were significantly upregulated after hypoxia exposure. Integrated analysis found that ho , igfbp1 , hsp70 , and hk2 were predicted to be regulated by novel_867, dre‐miR‐125c‐3p/novel_173, dre‐miR‐181b‐5p, and dre‐miR‐338‐5p/dre‐miR‐17a‐3p, respectively, and targets of DE miRNAs were significantly enriched in MAPK signaling pathway, FoxO signaling pathway, and glycolysis/gluconeogenesis. Expression analysis showed that the mRNA levels of vegfa , epo , ho , hsp70 , hsp90aa.1 , igfbp1 , ldh , hk1 , pfk , pk , and gapdh exhibited a remarkable increase, whereas sdh and mdh were downregulated in the H3h, H12h, and H24h groups compared with the control. Furthermore, research found that hk2 is a target of dre‐miR‐17a‐3p, overexpression of dre‐miR‐17a‐3p significantly decreased the expression level of hk2 , while the opposite results were obtained after dre‐miR‐17a‐3p silencing. These results contribute to our understanding of the molecular mechanisms of hypoxia tolerance in crucian carp.

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by significant difficulties in social interaction, communication, and repeated stereotypic behaviour. Aflatoxin B₁ (AFB₁) is the most potent and well-known mycotoxin in various food sources. Despite its propensity to generate significant biochemical and structural changes in human and animal tissues, the influence of AFB₁ on ASD has yet to be thoroughly studied. Mounting evidence indicates that chemokine receptors play a crucial function in the central nervous system and are implicated in developing several neuroinflammatory disorders. Chemokine receptors in individuals with ASD were elevated in the anterior cingulate gyrus astrocytes, cerebellum, and brain.

The BTBR T⁺Itpr3^tf/J (BTBR) mice are inbred strains that exhibit strong and consistently observed deficits in social interactions, characterized by excessive self-grooming and limited vocalization in social contexts. We examined the impact of AFB₁ on CCR3-, CCR7-, CCR9-, CXCR3-, CXCR4-, and CXCR6-expressing I-A/I-E⁺ cells in the spleen of the BTBR mouse model of autism. We evaluated the mRNA levels of CCR3, CCR7, CCR9, CXCR3, CXCR4, and CXCR6 chemokine receptors in the brain.

The exposure to AFB₁ in BTBR mice resulted in a significant rise in the number of I-A/I-E⁺CCR3⁺, I-A/I-E⁺CCR7⁺, I-A/I-E⁺CCR9⁺, I-A/I-E⁺CXCR3⁺, I-A/I-E⁺CXCR4⁺, and I-A/I-E⁺CXCR6⁺ cells. Furthermore, exposure to AFB₁ increased mRNA expression levels of CCR3, CCR7, CCR9, CXCR3, CXCR4, and CXCR6 in the brain.

These findings highlight that AFB₁ exposure increases the expression of chemokine receptors in BTBR mice, indicating the necessity for further research into AFB₁'s role in the development of ASD.