Biological Sciences and Engineering

Indian Institute of Technology Palakkad&nbsp;(IIT Palakkad or IIT PKD) is a public autonomous&nbsp;engineering&nbsp;and&nbsp;research&nbsp;institute located in&nbsp;Palakkad,&nbsp;Kerala. It was&nbsp;one of the five new&nbsp;IITs&nbsp;proposed in the&nbsp;2014 Union budget of India. The campus was inaugurated on 3 August 2015. The institute has 94 faculty, 978 students, and 63 non-teaching staffs.

IT Palakkad currently offers four-year Bachelor of Technology (B.Tech) and two years MS programmes in 8 different engineering disciplines including&nbsp;Computer Science, Electrical, Mechanical, Civil among others.

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IIT Palakkad

CD4 + CD25 + FoxP3 + regulatory T cells (Tregs) are exploited by mycobacteria to subvert the protective host immune responses. The Treg expansion in the periphery requires signaling by professional antigen presenting cells and in particularly dendritic cells (DC). However, precise molecular mechanisms by which mycobacteria instruct Treg expansion via DCs are not established. Here we demonstrate that mycobacteria-responsive sonic hedgehog (SHH) signaling in human DCs leads to programmed death ligand-1 (PD-L1) expression and cyclooxygenase (COX)-2-catalyzed prostaglandin E 2 (PGE 2) that orchestrate mycobacterial infection-induced expansion of Tregs. While SHH-responsive transcription factor GLI1 directly arbitrated COX-2 transcription, specific microRNAs, miR-324-5p and miR-338-5p, which target PD-L1 were downregulated by SHH signaling. Further, counter-regulatory roles of SHH and NOTCH1 signaling during mycobacterial-infection of human DCs was also evident. Together, our results establish that Mycobacterium directs a fine-balance of host signaling pathways and molecular regulators in human DCs to expand Tregs that favour immune evasion of the pathogen.

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Scientific Reports

Mycobacteria-responsive sonic hedgehog signaling mediates programmed death-ligand 1-and prostaglandin e 2-induced regulatory T cell expansion

Oncotarget

Cross-presentation of antigens by dendritic cells: Role of autophagy

CMAJ

Intravenous immunoglobulin as clinical immune-modulating therapy

Clinical Reviews in Allergy and Immunology

Erratum: Intravenous Immunoglobulin and Dendritic Cells [Clinic Rev Allerg Immunol, (29), (2005), 201-205, DOI 10.1385/CRIAI:29:3:201]

Single stranded DNA fragments were conjugated onto gold nanoparticles leading to the formation of gold nanoparticle clusters upon hybridization with complementary strands. These clusters were successfully implemented for signal amplification in an electrochemical DNA sensor based on a graphene substrate. The sensor exhibited excellent sensitivity and selectivity with a detection limit of 50 attomolar target DNA.

Analyst

A highly sensitive DNA sensor for attomolar detection of the BRCA1 gene: Signal amplification with gold nanoparticle clusters

Journal of Rheumatology

Erratum: Intravenous immunoglobulin expands regulatory T cells in autoimmune rheumatic disease (Letter) (Journal of Rheumatology (2012) 39 (450-452))

Despite promising clinical trials, intravenous immunoglobulin (IVIg) therapy in relapsing-remitting multiple sclerosis (MS) has met with uncertainties that might be attributed to small patient cohorts, heterogeneity in the patients, dose of IVIg, or the duration and window of treatment. © 2015 Elsevier Ltd. All rights reserved.

Trends in Pharmacological Sciences

IVIg for relapsing-remitting multiple sclerosis: Promises and uncertainties

Cellular and Molecular Immunology

Intravenous immunoglobulin-mediated expansion of regulatory T cells in autoimmune patients is associated with increased prostaglandin E2 levels in the circulation

T-helper (Th) 17 cells that express lineage-specific transcription factor RORC and produce cytokines interleukin 17A (IL-17A), interleukin 17F (IL-17F), and interleukin 22 (IL-22), play a key role in the clearance of both intracellular and extracellular bacteria and fungal infections. However, in the context of certain other infections, such as hepatitis B, chronic toxoplasmic uveitis, encephalitis, and Theiler murine encephalomyelitis, chronic activation of Th17 cells could contribute to tissue damage and immunopathology [1–3]. In line with these observations, Mbow et al [4] recently demonstrated that Th17 cells are associated with pathology in human schistosomiasis. They found elevated Th17 cells in peripheral blood of patients with schistosomiasis as well as in the liver and spleen of Schistosoma mansoni–infected mice. However, considering the essential role of innate immune cells in mediating T-cell responses, questions regarding the identification of innate cells that could promote Th17 responses during Schistosoma infection remain unexplored.In this regard, dendritic cells (DCs) are innate immune cells extensively studied for their role in antigen presentation and in the regulation of T-cell responses to pathogens. However, there is also growing evidence to implicate basophils in eliciting immune responses against helminth parasites including schistosomes. Basophils were recruited rapidly to the lymph nodes after exposure to S. mansoni eggs [5]. Because both DCs and basophils have important roles in regulating immune responses to pathogens, we sought to explore which of the innate cells are implicated in driving Th17 responses to schistosomes, as reported by Mbow et al [4].Dendritic cells were generated from peripheral blood monocytes, and basophils were isolated from peripheral blood mononuclear cells of healthy donors, as described elsewhere [6]. The S. mansoni eggs were obtained from 3–4 livers of golden hamsters infected with parasite cercarial larvae for 40 days [7]. The cell suspension was washed 3 times with Hank's balanced salt solution followed by collagenase B (100 µg/mL) treatment. The egg pellet was washed again with phosphate-buffered saline 3 times at 400 g for 1 minute. Eggs were counted, and the absence of contaminating hamster tissue fragments in the egg preparation was verified by microscopic analysis. CD4+ T cells were isolated from peripheral blood mononuclear cells by negative selection using a CD4+ T-cell isolation kit (Miltenyi Biotec). Regulatory T cells were removed by using CD25 microbeads (Miltenyi Biotec), and CD4+CD25− T cells were used for the experiments.To investigate the differential effect of DCs and basophils to promote Th17 responses to schistosomes, either untreated or S. mansoni egg–treated DCs and basophils were cocultured with autologous CD4+CD25− T cells. After 4 days of culture, Th17 responses were analyzed by means of flow cytometry (BD LSR II) and measurement of Th17 cytokines in the cell-free culture supernatants.

The Journal of Infectious Diseases

Mediation of T-Helper 17 Responses to Schistosomes by Dendritic Cells but Not Basophils

Journal of Infectious Diseases

Inhibition of programmed death 1 ligand 1 on dendritic cells enhances mycobacterium-mediated interferon γ (IFN-γ) production without modulating the frequencies of IFN-γ-producing CD4+ T cells