GATA binding protein 3+ group 2 innate lymphoid cells are present in cord blood and in higher proportions in male than in female neonates

Forsberg, Anna; Bengtsson, Mathias; Eringfält, Anna; Ernerudh, Jan; Mjösberg, Jenny; Jenmalm, Maria C.

doi:10.1016/j.jaci.2014.01.027

Cited by 24 publications

(16 citation statements)

References 9 publications

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“…However, given the inability of ILC2s to protect in WT females, the functionality of these cells also depends on male-specific influences (hormones, microbiota, chromosomes, etc.). Although not yet well documented in humans, it is notable that these differences in ILC2 populations are also observed in the umbilical cord blood of newborns, where males have an increased frequency of ILC2s (25). Taken together with our novel observations, these data provide new avenues for investigation into sex-determined disease susceptibility.…”

Section: Resultsmentioning

confidence: 99%

Cutting Edge: c-Kit Signaling Differentially Regulates Type 2 Innate Lymphoid Cell Accumulation and Susceptibility to Central Nervous System Demyelination in Male and Female SJL Mice

Russi

Walker-Caulfield

Ebel

et al. 2015

The Journal of Immunology

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Multiple sclerosis (MS) preferentially affects women and this sex dimorphism is recapitulated in the SJL mouse model of MS, experimental autoimmune encephalomyelitis (EAE). Here we demonstrate that signaling through c-kit exerts distinct effects on EAE susceptibility in male and female SJL mice. Previous studies in females show that Kit mutant (W/Wv) mice are less susceptible to EAE than wildtype mice. However, male W/Wv mice exhibit exacerbated disease, a phenotype independent of mast cells and corresponding to a shift from a Th2 to a Th17 dominated T cell response. We demonstrate a previously undescribed deficit in c-kit+ type 2 innate lymphoid cells (ILC2s) in W/Wv mice. ILC2s are also significantly reduced in EAE-susceptible WT females indicating that both c-kit signals and undefined male-specific factors are required for ILC2 function. We propose that deficiencies in Th2-promoting ILC2s removes an attenuating influence on the encephalitogenic T cell response and therefore increases disease susceptibility.

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Section: Resultsmentioning

confidence: 99%

Cutting Edge: c-Kit Signaling Differentially Regulates Type 2 Innate Lymphoid Cell Accumulation and Susceptibility to Central Nervous System Demyelination in Male and Female SJL Mice

Russi

Walker-Caulfield

Ebel

et al. 2015

The Journal of Immunology

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“…In humans, both ILC2-like (Lin-CRTH2+CD127+ cells) and ILC3-like (Lin-CD127+NKp44+ expressing RORγt) subsets were found in the fetal gut at 14-17 weeks of gestation 134 . In addition, Group 2 ILCs (GATA3+ ILCs) have been detected in the umbilical cord blood of term neonates 135 . In mice, fetal RORγt+ ILC progenitors mature in the fetal liver environment 136, 137 in a Notch2-dependent manner 138 .…”

Section: Discussionmentioning

confidence: 99%

The immunophenotype of amniotic fluid leukocytes in normal and complicated pregnancies

Gomez‐Lopez

Romero

et al. 2018

American J Rep Immunol

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Problem The immune cellular composition of amniotic fluid is poorly understood. Herein, we determined the immunophenotype of amniotic fluid: 1) immune cells during the second and third trimester; 2) T cells and innate lymphoid cells (ILCs); and 3) immune cells during intra-amniotic infection/inflammation. Method of Study Amniotic fluid samples (n=57) were collected from women from 15-40 weeks of gestation without intra-amniotic infection/inflammation. Samples from women with intra-amniotic infection/inflammation were also included (n=9). Peripheral blood mononuclear cells from healthy adults were used as controls (n=3). Immunophenotyping was performed using flow cytometry. Results In the absence of intra-amniotic infection/inflammation, the amniotic fluid contained several immune cell populations from 15-40 weeks. Among these immune cells: 1) T cells and ILCs were greater than B cells and NK cells between 15 to 30 weeks; 2) T cells were most abundant between 15 to 30 weeks; 3) ILCs were most abundant between 15 to 20 weeks; 4) B cells were scarce between 15 to 20 weeks; yet, they increased and were constant after 20 weeks; 5) NK cells were greater between 15 to 30 weeks than at term; 6) ILCs expressed high levels of RORγt, CD161, and CD103 (i.e. Group 3 ILCs); 7) T cells expressed high levels of RORγt; 8) neutrophils increased as gestation progressed; and 9) monocytes/macrophages emerged after 20 weeks and remained constant until term. All of the amniotic fluid immune cells, except ILCs, were increased in the presence of intra-amniotic infection/inflammation. Conclusions The amniotic fluid harbors a diverse immune cellular composition during normal and complicated pregnancies.

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“…Evidence that rhinovirus infection in neonatal but not adult mice drives the production of IL‐25 and expansion of ILC2s further suggests these cells might have a critical role in the development of allergic asthma in particular. Group 2 ILCs have been demonstrated in umbilical cord blood, and while there was a sex difference in their abundance, with newborn boys having more than newborn girls, there was no association with allergic outcomes in the small series of samples studied . Cytokine outputs were not studied, and it will be of interest to investigate potential functional differences in these cells and allergic disease outcomes.…”

Section: Immune Responses In Utero and Early Lifementioning

confidence: 99%

Mechanisms of allergic disease – environmental and genetic determinants for the development of allergy

Campbell

Boyle

Thornton

et al. 2015

Clin Experimental Allergy

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Summary Allergic disease can be viewed as an early manifestation of immune dysregulation. Environmental exposures including maternal inflammation, diet, nutrient balance, microbial colonization and toxin exposures can directly and indirectly influence immune programming in both pregnancy and the postnatal period. The intrauterine microclimate is critical for maternal and fetal immunological tolerance to sustain viable pregnancy, but appears susceptible to environmental conditions. Targeting aspects of the modern environment that promote aberrant patterns of immune response is logical for interventions aimed at primary prevention of allergic disease. Defining the mechanisms that underpin both natural and therapeutic acquisition of immunological tolerance in childhood will provide insights into the drivers of persistent immune dysregulation. In this review, we summarize evidence that allergy is a consequence of intrauterine and early life immune dysregulation, with specific focus on contributing environmental risk factors occurring preconception, in utero and in the early postnatal period. We explore the immunological mechanisms which underpin tolerance and persistence of allergic disease during childhood. It is likely that future investigations within these two domains will ultimately provide a road map for the primary prevention of allergic disease.

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GATA binding protein 3+ group 2 innate lymphoid cells are present in cord blood and in higher proportions in male than in female neonates

Cited by 24 publications

References 9 publications

Cutting Edge: c-Kit Signaling Differentially Regulates Type 2 Innate Lymphoid Cell Accumulation and Susceptibility to Central Nervous System Demyelination in Male and Female SJL Mice

Cutting Edge: c-Kit Signaling Differentially Regulates Type 2 Innate Lymphoid Cell Accumulation and Susceptibility to Central Nervous System Demyelination in Male and Female SJL Mice

The immunophenotype of amniotic fluid leukocytes in normal and complicated pregnancies

Mechanisms of allergic disease – environmental and genetic determinants for the development of allergy

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