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D'Cruz, L. M.

Publications and source records attributed to D'Cruz, L. M..

4 recordsLinked to original sources

A high-resolution blood immune cell doublet atlas via imaging spectral cytometry

Circulating cell-cell complexes (doublets) provide critical insights into in vivo immune interactions. Here, we leverage high-dimensional imaging spectral cytometry to systematically map the landscape of immune doublets in human peripheral blood. By integrating morphometric imaging features with a 22-color spectral panel, we established a gating workflow that cleanly segregates genuine, physically interacting complexes from coincidental transits and platelet contaminants, and resolved 12 highly pure homotypic and heterotypic immune doublet configurations in peripheral blood mononuclear cells (PBMC). At steady state, each doublet population displayed unique abundance, affinity and surface phenotypic profiles relative to circulating singlets. Principal component analysis (PCA) of quantitative imaging features further revealed lineage-specific topologies distinguishing singlet cells, homotypic doublets, and heterotypic pairs. Finally, comparative cohort analysis demonstrated that while doublet frequencies, affinities and surface phenotypes remain comparable between healthy donors and patients with tuberculosis (TB) disease, imaging-derived features uncovered disease-specific alterations in doublets morphology. Specifically, high-dimensional clustering using imaging parameters showed that TB disease significantly enriches for a tightly synapsed T cell-monocyte cluster characterized by high CD3-CD14 pixel correlation. Collectively, this study establishes a robust framework for mapping circulating cell-cell networks and demonstrates the superior sensitivity of imaging features over conventional fluorescence for capturing functional immune interactions in health and disease.

immunology↗

Blimp-1 in adipose resident Tregs controls adipocyte beiging and obesity

Crosstalk between the immune system and adipocytes is critical for maintaining tissue homeostasis and regulating chronic systemic inflammation during diet-induced obesity (DIO). How visceral adipose tissue resident regulatory T cells (aTregs) signal to adipocytes in the visceral adipose tissue (VAT) is not understood. Here we show that Treg-specific ablation of the transcriptional regulator Blimp-1 resulted in increased insulin sensitivity, decreased body weight and increased Ucp-1 in adipocytes in high fat diet (HFD)-fed mice. Mechanistically, we demonstrate that Blimp-1 drives IL-10 production in Tregs, thus suppressing beiging and energy expenditure in adipocytes. Moreover, IL-10 mRNA expression positively correlated with increasing body weight in humans. These findings reveal a surprising relationship between aTregs and adipocytes in promoting insulin resistance during excessive caloric intake, placing Blimp-1-regulated IL-10 expression by aTregs at a critical juncture in the development of obesity and its associated comorbidities in mice and humans. SUMMARYHere we show that ablation of Blimp-1 in adipose tissue resident Tregs (aTregs) leads to decreased IL-10 production, resulting in increased Ucp-1 expression and beiging by adipocytes and protection from diet-induced obesity and insulin resistance.

immunology↗

The transcriptional regulator Id2 is critical for adipose-resident regulatory T cell differentiation, survival and function

Adipose regulatory T cells (aTregs) have emerged as critical cells for the control of local and systemic inflammation. In this study, we show a distinctive role for the transcriptional regulator Id2 in the differentiation, survival and function of aTregs. Id2 was highly expressed in aTregs compared with high Id3 expression in lymphoid Tregs. Treg-specific deletion of Id2 resulted in a substantial decrease in aTregs, while Tregs in the spleen and lymph nodes were unaffected. Additionally, loss of Id2 resulted in decreased expression of aTreg associated markers including ST2, CCR2, KLRG1 and GATA3. Gene expression analysis revealed that Id2 expression was essential for the survival of aTregs and loss of Id2 increased cell death in aTregs due to increased Fas expression. Id2-mediated aTreg depletion resulted in increased systemic inflammation, increased inflammatory macrophages and CD8+ effector T cells and loss of glucose tolerance under standard diet conditions. Thus, we reveal an unexpected and novel function for Id2 in mediating differentiation, survival and function of adipose-resident Tregs, that when lost resulting in increased metabolic perturbation.

immunology↗

PIK3IP1/TrIP restricts activation of T cells through inhibition of PI3K/Akt

Phosphatidylinositol-3 kinases (PI3Ks) modulate numerous cellular functions, including growth, proliferation and survival. Dysregulation of the PI3K pathway can lead to autoimmune disease and cancer. PIK3IP1 (or Transmembrane Inhibitor of PI3K - TrIP) is a novel transmembrane regulator of PI3K. TrIP contains an extracellular kringle domain and an intracellular \"p85-like\" domain with homology to the inter-SH2 domain of the regulatory subunit of PI3K. Although TrIP has been shown to bind to the p110 catalytic subunit of PI3K in fibroblasts, the mechanism by which TrIP functions is poorly understood. We show that both the kringle and \"p85-like\" domains are necessary for TrIP inhibition of PI3K. We also demonstrate that TrIP protein is down-modulated from the surface of T cells to allow T cell activation. In addition, we present evidence that the kringle domain may modulate TrIP function by binding an as-yet-unidentified ligand. Using an inducible knockout mouse model that we developed, we show that TrIP-deficient T cells exhibit more robust T cell activation, show a preference for Th1 polarization and can mediate clearance of Listeria monocytogenes infection faster than WT mice. Thus, TrIP is an important negative regulator of T cell activation and may represent a novel target for immune modulation therapies.

immunology↗