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soluble CD48 levels were significantly elevated in patients with nonallergic asthma compared to control and to the allergic asthma cohort
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mCD48 and sCD48 are differentially expressed in the peripheral blood of asthma patients of varying severity. sCD48 inhibits CD244-mediated eosinophil activation. These findings suggest that CD48 may play an important role in human asthma.
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The present study provides further insights into the role of the 2B4-CD48 interaction in the fine regulation of CD8(+) T-cell effector function upon antigenic stimulation.
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Data show that 2B4 not only can bind to CD48 in trans but also interacts with CD48 in cis by using the same binding interface. Also, the results demonstrated that constitutive phosphorylation of 2B4 occurs only in the presence of CD48, and that cis binding is sufficient to induce substantial levels of baseline phosphorylation.
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Our data indicate sCD48 as a SEB-induced 'decoy' receptor derived from eosinophil and therefore as a potential anti-inflammatory tool in S. aureus-induced eosinophil inflammation often associated with allergy.
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CD48 expression was increased in patients with a short disease duration compared to both controls and patients with longer disease duration. In patients with short disease duration, increased CD48 expression was associated with alveolar inflammation.
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These data demonstrate the important role of CD48 in SA/exotoxins-eosinophil activating interactions that can take place during allergic responses and indicate CD48 as a novel therapeutic target for allergy and especially of AD.
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Blockade of 2B4/CD48 interaction resulted in improvement in function via perforin expression and degranulation as measured by CD107a surface mobilization on HTLV-1 specific CD8+ T cells.
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we propose that SLAMF2 engagement regulates adaptive immune responses
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Monocyte-induced natural killer cell dysfunction was markedly attenuated by blocking CD48 receptor 2B4 on NK cells, but not by blockade of NKG2D and NKp30.
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replication study of association of 2 SNPs in HERV-K18 and 19 tagSNPs in CD48 with schizophrenia (SZ)and type 2 diabetes (T2D) in patients with SZ in 2 Danish samples; no association was found with SZ or with T2D among individuals with SZ for any of the SNPs
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Stimulation of CD48 induces rearrangement of signaling factors in lipid rafts, Lck-kinase activity, and tyrosine phosphorylation.
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The ligand (CD48) of the 2B4 receptor can exert both activating and inhibiting signals; natural killer (NK) cells might be at risk for self-killing were it not for the inhibiting signals generated by the 2B4-CD48 interaction.
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CM1-induced apoptosis is achieved via different initiation pathways, which are cell-type dependent
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Signal-dependent adhesion of resting NK cells initiated by expression of ICAM-1 is greatly enhanced by coexpression of CD48, even in the absence of cytokines.
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Engagement of natural killer (NK) cell receptor 2B4 by its counterreceptor, CD48, expressed on target cells leads to an inhibition in NK cytotoxicity independent of signaling lymphocytic activation molecule-associated protein (SAP) expression.
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IL-18, IL-18 receptor alpha, and CD48 complex formation via glycosylphosphatidylinositol anchor glycan triggers binding to IL-18 receptor beta, and thereby induces intracellular signal transduction and IFN-gamma production.
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Review of recent studies suggests an important role for interactions between 2B4 and CD48 in the course of T cell activation and proliferation
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2B4 (CD244) can stimulate NK cell cytotoxicity and cytokine production by interacting with NK cell expressed CD48 and adds CD48 to the growing number of activating NK cell receptors
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CD48 is an interleukin (IL)-3-induced activating receptor on eosinophils and may be involved in promoting allergic inflammation.
