Almin Lalani

ORCID: 0000-0003-3418-6571
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About
Contact & Profiles
Research Areas
  • Cancer Immunotherapy and Biomarkers
  • CAR-T cell therapy research
  • Immunotherapy and Immune Responses
  • Cancer Genomics and Diagnostics
  • Genetic factors in colorectal cancer
  • Immune Response and Inflammation
  • Monoclonal and Polyclonal Antibodies Research
  • Immune cells in cancer
  • NF-κB Signaling Pathways
  • interferon and immune responses
  • Inflammation biomarkers and pathways
  • Cytokine Signaling Pathways and Interactions
  • Pharmacological Effects of Natural Compounds
  • Cancer Research and Treatments
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Ubiquitin and proteasome pathways
  • Immunodeficiency and Autoimmune Disorders
  • Lymphoma Diagnosis and Treatment
  • Inflammatory Biomarkers in Disease Prognosis
  • vaccines and immunoinformatics approaches
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cancer, Stress, Anesthesia, and Immune Response
  • Neuroscience and Neuropharmacology Research

Rutgers, The State University of New Jersey
2013-2025

PCR Oncology
2023

Amgen (United States)
2020-2022

National Institutes of Health
2021

National Cancer Institute
2021

Rutgers Sexual and Reproductive Health and Rights
2016-2019

Abstract Immunotherapies can mediate regression of human tumors with high mutation rates, but responses are rarely observed in patients common epithelial cancers. This raises the question whether these cancers harbor T lymphocytes that recognize mutant proteins expressed by autologous may represent ideal targets for immunotherapy. Using high-throughput immunologic screening gene products identified via whole-exome sequencing, we neoantigen-reactive tumor-infiltrating (TIL) from 62 75 (83%)...

10.1158/2159-8290.cd-18-1494 article EN Cancer Discovery 2019-06-04

Abstract Microglia, the resident immune cells of brain, perform elaborate surveillance in which they physically interact with neuronal elements. A novel form microglia–neuron interaction named microglial process convergence (MPC) toward axons and dendrites has recently been described. However, molecular regulators pathological relevance MPC have not explored. Here, using high-resolution two-photon imaging vivo ex , we observed a dramatic increase MPCs after kainic acid– or...

10.1523/eneuro.0209-16.2016 article EN cc-by-nc-sa eNeuro 2016-11-01

Inhibitors that block the programmed cell death-1 (PD-1) pathway can potentiate endogenous antitumor immunity and have markedly improved cancer survival rates across a broad range of indications. However, these treatments work for only minority patients. The efficacy anti-PD-1 inhibitors may be extended by cytokines, however, incorporation cytokines into therapeutic regimens has significant challenges. In their natural form when administered as recombinant proteins, cytokine are often...

10.3389/fimmu.2020.00832 article EN cc-by Frontiers in Immunology 2020-05-08

Abstract Purpose: Immune checkpoint blockade (ICB) agents and adoptive cell transfer (ACT) of tumor-infiltrating lymphocytes (TIL) are prominent immunotherapies used for the treatment advanced melanoma. Both therapies rely on activation that target shared tumor antigens or neoantigens. Recent analysis patients with metastatic melanoma who underwent TIL ACT at NCI demonstrated decreased responses in previously treated anti–PD-1 agents. We aimed to find a basis difference response rates...

10.1158/1078-0432.ccr-21-4499 article EN Clinical Cancer Research 2022-03-03

Myeloid cells, including granulocytes, monocytes, macrophages, and dendritic are crucial players in innate immunity inflammation. These cells constitutively or inducibly express a number of receptors the TNFR TLR families, whose signals transduced by TNFR-associated factor (TRAF) molecules. In vitro studies showed that TRAF3 is required for TLR-induced type I IFN production, but vivo function myeloid remains unknown. this article, we report generation characterization cell-specific...

10.4049/jimmunol.1401548 article EN The Journal of Immunology 2014-11-25

Abstract Myeloid cells are central players in innate immunity and inflammation. Their function is regulated by the adaptor protein TRAF3. We previously reported that aging myeloid cell-specific TRAF3-deficient (M-Traf3-/-) mice spontaneously develop chronic inflammation B-cell lymphoma (BCL). In present study, we aimed to identify internal trigger of this disease phenotype these mice. first detected gut dysbiosis transmigration commensal bacteria liver M-Traf3-/- Interestingly, depletion...

10.1158/1538-7445.am2025-2217 article EN Cancer Research 2025-04-21

Tumor necrosis factor receptor-associated 3 (TRAF3), a member of the TRAF family cytoplasmic adaptor proteins with E3 ligase activity, is ubiquitously expressed in various cell types immune system. It shared for signaling by variety adaptive and innate receptors as well cytokine receptors. Previous studies examining conditional TRAF3-deficient mouse models that have Traf3 gene specifically deleted B lymphocytes or T revealed diverse critical vivo functions TRAF3 immunity. Although vitro...

10.14800/macrophage.1009 article EN Macrophage 2015-10-27

While the rapid advancement of immunotherapies has revolutionized cancer treatment, only a small fraction patients derive clinical benefit. Eradication large, established tumors appears to depend on engaging and activating both innate adaptive immune system components mount rigorous comprehensive response. Identifying such agents is high unmet medical need, because they are sparse in therapeutic landscape treatment. Here, we report that IL-36 cytokine can engage immunity remodel an...

10.1172/jci162088 article EN cc-by Journal of Clinical Investigation 2023-06-14

Myeloid-derived suppressor cells (MDSCs) are aberrantly expanded in cancer patients and under other pathological conditions. These orchestrate the immunosuppressive inflammatory network to facilitate metastasis mediate patient resistance therapies, thus recognized as a prime therapeutic target of human cancers. Here we report identification adaptor protein TRAF3 novel immune checkpoint that critically restrains MDSC expansion. We found myeloid cell-specific Traf3 -deficient (M- -/- ) mice...

10.3389/fimmu.2023.1167924 article EN cc-by Frontiers in Immunology 2023-05-03

Antibodies, also termed as immunoglobulins (Ig), secreted by differentiated B lymphocytes, plasmablasts/plasma cells, in humoral immunity provide a formidable defense against invading pathogens via diverse mechanisms. One major goal of vaccination is to induce protective antigen-specific antibodies prevent life-threatening infections. Both thymus-dependent (TD) and thymus-independent (TI) antigens can elicit robust IgM responses the production isotype-switched (IgG, IgA IgE) well generation...

10.3791/57843 article EN Journal of Visualized Experiments 2018-09-07

<div>AbstractPurpose:<p>Immune checkpoint blockade (ICB) agents and adoptive cell transfer (ACT) of tumor-infiltrating lymphocytes (TIL) are prominent immunotherapies used for the treatment advanced melanoma. Both therapies rely on activation that target shared tumor antigens or neoantigens. Recent analysis patients with metastatic melanoma who underwent TIL ACT at NCI demonstrated decreased responses in previously treated anti–PD-1 agents. We aimed to find a basis difference...

10.1158/1078-0432.c.6532607.v1 preprint EN 2023-03-31

Abstract Myeloid cells are the major players of innate immunity and inflammation. The function myeloid is critically regulated by adaptor protein TRAF3. We previously reported that aging cell-specific TRAF3-deficient (M-Traf3-/- ) mice spontaneously develop chronic inflammation B-cell lymphoma (BCL). Here we sought to identify internal trigger aberrant B cell activation in these mice. first detected gut dysbiosis transmigration commensal bacteria liver M-Traf3-/- using 16s rRNA gene...

10.1158/2643-3249.lymphoma24-po-018 article EN Blood Cancer Discovery 2024-06-19

Abstract TRAF3 is a new tumor suppressor gene in B lymphocytes. Deletions and mutations of were detected human non-Hodgkin lymphoma (NHL) multiple myeloma (MM). We previously reported that specific deletion lymphocytes causes prolonged survival mature cells, which eventually leads to development mice. Here we identified Rhbdf1, 7-transmembrane domain protein implicated the trafficking ER proteins, as novel target inactivation cells. Rhbdf1 expression was strikingly up-regulated...

10.4049/jimmunol.198.supp.212.2 article EN The Journal of Immunology 2017-05-01

Abstract TRAF3, a cytoplasmic adaptor protein, is used in signaling by the TNFR superfamily and pattern recognition receptors. A number of these receptors are constitutively or inducibly expressed myeloid cells, crucial players innate immunity inflammation. To investigate vivo functions TRAF3 we generated cell-specific TRAF3-/- (M-TRAF3-/-; TRAF3flox/floxLysM+/Cre) mice. We previously showed that young adult M-TRAF3-/- mice have normal frequencies numbers lymphocyte cell populations lymphoid...

10.4049/jimmunol.194.supp.192.6 article EN The Journal of Immunology 2015-05-01

Abstract Myeloid cells, including monocytes, macrophages and granulocytes, are crucial players of innate immunity inflammation. These cells constitutively or inducibly express a number receptors the TNF receptor superfamily Toll-like (TLRs), whose signals transduced by TRAF molecules. In light in vitro evidence that TRAF3 is required for TLRs-induced type I interferon production CD40-induced IL-12 macrophages, we generated myeloid cell-specific TRAF3-/- (M-TRAF3-/-; TRAF3flox/floxLysM+/Cre)...

10.4049/jimmunol.190.supp.188.2 article EN The Journal of Immunology 2013-05-01

<div>AbstractPurpose:<p>Immune checkpoint blockade (ICB) agents and adoptive cell transfer (ACT) of tumor-infiltrating lymphocytes (TIL) are prominent immunotherapies used for the treatment advanced melanoma. Both therapies rely on activation that target shared tumor antigens or neoantigens. Recent analysis patients with metastatic melanoma who underwent TIL ACT at NCI demonstrated decreased responses in previously treated anti–PD-1 agents. We aimed to find a basis difference...

10.1158/1078-0432.c.6532607 preprint EN 2023-03-31
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