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The regulation of T cell proliferation during HPIV3 infection is mediated via NK receptors NKp44 and NKp46 and involves the surface glycoprotein haemagglutinin-neuraminidase but not the fusion protein of the virus.
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Study identified a novel ligand for NKp44 on astrocytes. Expression of this novel ligand decreased with increasing HIV-3S peptide concentration and blocking this novel ligand decreased NK cell killing. NK cell killing of astrocytes was decreased when astrocytes were incubated with HIV-3S peptide. NKp44 has a protective effect on astrocytes from NK cell mediated killing during HIV infection and impact astrocyte's role.
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NKp44 and NKp30 splice variants profiles are tissue/condition specific and demonstrate similarity between placenta and cancerous tissues.
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NKp44-1 expression was significantly associated with poor survival of AML patients. Moreover, activation of PBMC from healthy controls showed co-dominant expression of NKp44-1 and NKp44-3, while primary NK clones show more diverse NKp44 splice variant profiles.
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On CD56(+) CD3(-) cells, NKp44 and NKp46 expressions were high in the acute hepatitis E patients, whereas NKp30, NKp44, NKp46 and NKG2D were high in the recovered individuals.
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demonstrated that the mitogen and iK562 exposure to peripheral blood mononuclear cells can significantly improve NK activity which is co-related to the higher expression of NKp44 and NKG2D
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NCR(+) ILC3 from skin and blood of psoriasis patients produced IL-22, which is regarded as a key driver of epidermal thickening, suggesting that NCR(+) ILC3 may participate in psoriasis pathology.
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Balance between activating NKG2D, DNAM-1, NKp44 and NKp46 and inhibitory CD94/NKG2A receptors determine natural killer degranulation towards rheumatoid arthritis synovial fibroblasts.
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NKp44+ ILC3 are expressed in human skin and blood and may have a role in psoriasis pathogenesis
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Expression of NKp44 ligand by normal articular chondrocytes is not involved in their killing by unstimulated NK cells; however, it is responsible for anti-chondrocyte cytotoxicity mediated by long-term activated NK cells.
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MLL5 is a cellular ligand for the natural cytotoxicity receptor NKp44.
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Natural killer cells in HIV controller patients express an activated effector phenotype and do not up-regulate NKp44 on IL-2 stimulation.
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Novel interaction between proliferating cell nuclear antigen and HLA I on the surface of tumor cells inhibits NK cell function through NKp44.
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triggering in RORgammat-positive innate lymphoid cells selectively activates a proinflammatory program
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While interaction of TLR2 with mycobacterial cell wall promotes activation of resting NK cells and IFN-gamma production, NKp44 interaction with its putative ligands could play a secondary role in maintaining cell activation
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Natural cytotoxicity receptors play a major role in the recognition by NK cells of cancer stem cells targets.
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These data show that the Kaposi's sarcoma-associated herpesvirus ORF54 product downregulates the NKp44 ligand and that the NKp44-NKp44 ligand signaling pathway contributes to antiviral immunity.
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a precise analysis of clinical data showed a correlation between decreased NCR expression and poor prognosis factors such as low haemoglobin level, high (>30x10(9) per litre) lymphocyte count or elevated C-reactive protein
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We demonstrate that PCNA promotes cancer survival by immune evasion through inhibition of NKp44-mediated NK cell attack.
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Data show that pDCs isolated from peripheral blood of systemic lupus erithematosus (SLE) patients express lower levels of LAIR-1 while displaying slight but consistent expression of NKp44.
