Introduction: Fc receptor-like (FCRL) molecules, as recently identified members of the immunoglobulin superfamily (IgSF), are preferentially expressed by B-cells. They have variable number of extracellular immunoglobulin-like domains and cytoplasmic activating ITAMs and/or inhibitory ITIMs. FCRL1-5 are dominantly expressed in different stages of B-cells development. But, FCRL6 is preferentially expressed in different subsets of T-cells and NK cells. FCRL1-5 could regulate different features of B-cell evolution such as development, differentiation, activation, antibody secretion and isotype switching. Areas covered: Improved understanding of FCRL expression may grant B-cells and finally its signaling pathways, alone or in cooperation with other signaling molecules, as interesting new targets for diagnostic, monitoring and immunotherapeutic modalities; although further investigations remain to be defined. Recent investigations on different family members of FCRL proteins have substantiated their differential expression on different tissues, malignancies, immune related disease and infectious diseases. Expert opinion: FCRLs restricted expressions in normal B-cells and T-cell subsets accompanied with their overexpression in B-cell malignancies introduce them as logical candidates for the development of antibody- and cell-based immunotherapy approaches in B-cell malignancies, immune-mediated and infectious diseases. FCRLs would be applied as attractive and specific targets for immunodiagnostic approaches, clinical prognosis as well as disease monitoring of relevant patients.

Background: Acinetobacter baumanniiis an opportunistic and antibiotic-resistant pathogen that predominantly causes nosocomial infections. There is urgent need for development nonantibiotic-based treatment strategies. We developed a novel monoclonal antibody (mAb) against a peptide of conserved outer membrane protein A (OmpA) and evaluated its reactivity with different pulsotypes ofA. baumannii.Methods: Peptide derived fromA. baumanniiOmpA was conjugated to keyhole limpet hemocyanin and injected into BALB/c mice. Splenocytes of immunized mice were fused with SP2/0 myeloma cells followed by selection of antibody-producing hybridoma cells. After screening of different hybridoma colonies by ELISA, one monoclone was selected as 3F10-C9 and the antibody was tested for reaction with five differentAcinetobacterpulsotypes that were resistant to carbapenem antibiotics. The affinity constant was measured by ELISA. The ELISA, western blotting, indirect immunofluorescence (IFA), and in vitro opsonophagocytosis assays were used to evaluate the reactivity of generated mAb.Results: The anti-OmpA antibody reacted with the immunizing peptide and had a high affinity (1.94 × 10⁻⁹ M) for its antigen in the ELISA. Specific binding of mAb to OmpA was confirmed in Western blot. IFA assays revealed that mAb recognized specific OmpA on the pulsotypes. Opsonophagocytosis assays showed that the mAb increased the bactericidal activity of macrophage cells. The antibody function was higher in the presence of serum complement.Conclusions: The peptide-based mAb demonstrated optimal performance in laboratory experiments which may be appropriate in investigation on OmpA inAcinetobacterpathogenesis and development of passive immunization as a novel therapeutic approach.

Non-Alcoholic Fatty Liver Disease (NAFLD) is a spectrum of liver diseases from simple steatosis to the most severe form of hepatocellular carcinoma. Liver injuries resulting from various factors, including viral infections, alcohol consumption, and metabolic disorders, trigger the activation of resident immune cells and the recruitment of circulating immune cells to the liver. This chronic inflammatory environment leads to tissue damage and the progression of liver fibrosis. Macrophages are highly versatile immune cells that play a dual role in fibrosis: they contribute to the progression of fibrosis (M1 and Ly6chigh macrophages) and its resolution (M2 and Ly6clow macrophages). M1 macrophages and those with high surface expression of Ly6C exhibit pro-inflammatory characteristics, while M2 macrophages and myeloid cells with low expression of Ly6C mitigate inflammation and inhibit fibrosis progression. Environmental stimuli influence the complex mechanisms hepatic macrophages regulate the fibrosis they encounter. Kupffer cells initiate the inflammatory cascade and recruit monocyte-derived macrophages, which modulate the propagation of fibrosis and promote fibrinolysis. Additionally, hepatic macrophages interact with other cell types through exosomes, facilitating the transfer of cellular components that influence the outcome of liver fibrosis. In this review, the critical role of macrophages in inflammation-induced fibrosis and tissue restoration is discussed.