Effect of CMV and Aging on the Differential Expression of CD300a, CD161, T-bet, and Eomes on NK Cell Subsets

López-Sejas, Nelson; Campos, Carmen; Hassouneh, Fakhri; Sánchez-Correa, Beatriz; Tarazona, Raquel; Pera, Alejandra; Solana, Rafael

doi:10.3389/fimmu.2016.00476

Cited by 29 publications

(21 citation statements)

References 82 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Age may also have a role in the increased percentage of CD300a+ cells, although the old subjects that participated in the study were all CMV seropositive . Just as in T cells, latent CMV infection and age induce significant changes in the expression of CD300a on NK cells .…”

Section: Cd300 Molecules and Cellular Responses To Viral Infectionsmentioning

confidence: 99%

CD300 receptor family in viral infections

et al. 2018

View full text Add to dashboard Cite

The CD300 molecules constitute an evolutionarily significant family of receptors that are expressed on myeloid and lymphoid cells, but also on other cell types, such as tuft cells. Many of the CD300 receptors have been shown to recognize lipids, e.g. phosphatidylserine and phosphatidylethanolamine. Over the past couple of years, accumulating evidence has shown that this family of receptors is involved in the pathogenesis of many diseases. Specifically, CD300 molecules participate in the mechanisms that viruses employ to develop immune evasion strategies and to infect host cells. The participation of CD300 molecules in viral infection includes both lipid dependent and independent mechanisms, as for example in infections with dengue virus (DENV) and murine norovirus (MNV), respectively. CD300 receptors are also involved in viral escape mechanisms, for instance inhibiting NK cell‐mediated cytotoxicity against infected cells. Moreover, it is becoming increasingly recognized that the expression of CD300 receptors is altered during viral diseases. Here, we review the involvement of human and murine CD300 molecules in viral binding and entry and in cellular responses to viruses, which highlights the potential of CD300 molecules in the search of new biomarkers for various stages of infection and therapeutic targets for the treatment of viral infections.

show abstract

Section: Cd300 Molecules and Cellular Responses To Viral Infectionsmentioning

confidence: 99%

CD300 receptor family in viral infections

et al. 2018

View full text Add to dashboard Cite

show abstract

“…These hallmarks include the age-associated deterioration of the immune response, also termed immunosenescence, and the existence of age-associated low-grade inflammation usually known as inflamm-ageing [ 25 ]. CMV infection is associated with immunosenescence and the accumulation of highly differentiated T cell clones [ 26 , 27 ] characterized by the production of pro-inflammatory cytokine [ 28 , 29 , 30 , 31 , 32 , 33 ]. One of the major hallmarks of immunosenescence is leukocyte telomere shortening [ 34 ].…”

Section: CMV Is a Major Driver Of Immunosenescencementioning

confidence: 99%

“…In addition, telomere shortening is more rapid in CMV-seropositive individuals, indicating that CMV infection induces a strong decrease in T cell telomere length [ 60 ]. CMV seropositivity and CMV IgG antibodies correlate not only with LTL but also with telomerase activity [ 61 ] The telomere lengths in total and CMV-specific T cells are shorter in old compared to young individuals, although the accumulated end-stage cells are multifunctional T cells and do not have the shortest telomeres [ 31 ]. CMV seropositivity and increased total pathogen burden level are significantly associated with shorter telomere length among females [ 62 ].…”

Section: CMV Is a Major Driver Of Immunosenescencementioning

confidence: 99%

Early Senescence and Leukocyte Telomere Shortening in SCHIZOPHRENIA: A Role for Cytomegalovirus Infection?

Solana¹,

Pereira²,

Tarazona

2018

Brain Sciences

Self Cite

View full text Add to dashboard Cite

Schizophrenia is a severe, chronic mental disorder characterized by delusions and hallucinations. Several evidences support the link of schizophrenia with accelerated telomeres shortening and accelerated aging. Thus, schizophrenia patients show higher mortality compared to age-matched healthy donors. The etiology of schizophrenia is multifactorial, involving genetic and environmental factors. Telomere erosion has been shown to be accelerated by different factors including environmental factors such as cigarette smoking and chronic alcohol consumption or by psychosocial stress such as childhood maltreatment. In humans, telomere studies have mainly relied on measurements of leukocyte telomere length and it is generally accepted that individuals with short leukocyte telomere length are considered biologically older than those with longer ones. A dysregulation of both innate and adaptive immune systems has been described in schizophrenia patients and other mental diseases supporting the contribution of the immune system to disease symptoms. Thus, it has been suggested that abnormal immune activation with high pro-inflammatory cytokine production in response to still undefined environmental agents such as herpesviruses infections can be involved in the pathogenesis and pathophysiology of schizophrenia. It has been proposed that chronic inflammation and oxidative stress are involved in the course of schizophrenia illness, early onset of cardiovascular disease, accelerated aging, and premature mortality in schizophrenia. Prenatal or neonatal exposures to neurotropic pathogens such as Cytomegalovirus or Toxoplasma gondii have been proposed as environmental risk factors for schizophrenia in individuals with a risk genetic background. Thus, pro-inflammatory cytokines and microglia activation, together with genetic vulnerability, are considered etiological factors for schizophrenia, and support that inflammation status is involved in the course of illness in schizophrenia.

show abstract

“…Age-related alterations in frequency, distribution, phenotype, and function of NK cell subsets have been described, including an increased expression of CD57 (considered a marker of ‘memory-like' NK) and a decreased expression of Natural Cytotoxicity Receptors (NCRs) and other NK activating receptors ( 22 , 23 , 28 – 31 ), CD69 ( 32 ), and CD94/NKG2A, and an increase of killer Ig-like receptors (KIR) ( 33 – 35 ) in older individuals.…”

Section: Introductionmentioning

confidence: 99%

Effect of Age on NK Cell Compartment in Chronic Myeloid Leukemia Patients Treated With Tyrosine Kinase Inhibitors

et al. 2018

Self Cite

View full text Add to dashboard Cite

Natural killer (NK) cells are a very important component of the innate immune response involved in the lysis of virus infected and tumor cells. Aging has a profound impact in the frequency, phenotype and function of NK cells. Chronic Myeloid Leukemia (CML) is caused by the BCR-ABL gene formation encoding aberrant oncoprotein tyrosine kinase. Treatment with tyrosine kinase inhibitors (TKIs) induces durable deep molecular response. The response to treatment and life expectancy is lower in older patients with chronic phase of CML than in younger patients. In this work we analyse NK cells from TKI-treated CML patients and healthy controls stratified according to age. We have analyzed the expression of NK receptors, activation markers, NK cell differentiation in CD56bright and CD56dim NK cell subsets and the expression of CD107a and IFN-γ in NK cells stimulated with K562. Whereas significant differences on the phenotype and function of NK cells were found between middle-aged (35–65 years old) and elderly (older than 65) healthy individuals, NK cells from TKI-treated CML patients do not show significant differences related with age in most parameters studied, indicating that age is not a limitation of the NK cell recovery after treatment with TKI. Our results also revealed differences in the expression of NK receptors, activation markers and functional assays in NK cells from TKI-treated CML patients compared with age-matched healthy controls. These results highlight the relevance of NK cells in TKI-treated patients and the need of an extensive analysis of the effect of aging on NK cell phenotype and function in these patients in order to define new NK-cell based strategies directed to control CML progression and achieve long-term disease remission after TKI cessation.

show abstract

Effect of CMV and Aging on the Differential Expression of CD300a, CD161, T-bet, and Eomes on NK Cell Subsets

Cited by 29 publications

References 82 publications

CD300 receptor family in viral infections

CD300 receptor family in viral infections

Early Senescence and Leukocyte Telomere Shortening in SCHIZOPHRENIA: A Role for Cytomegalovirus Infection?

Effect of Age on NK Cell Compartment in Chronic Myeloid Leukemia Patients Treated With Tyrosine Kinase Inhibitors

Contact Info

Product

Resources

About