Abstract: The present invention includes methods of treating cancer in a patient, the method comprising the steps of: (a) providing or obtaining a sample from a patient; (b) determining at least one of a level or activity of at least one of: T follicular regulatory (TFR), ST2 Treg, highly suppressive Treg, activated Treg, or effector Treg cells in the sample; (c) comparing the at least one level or activity of the T cells in the sample to a level or activity of the T cells in a reference sample, respectively, for a specific tumor type or a healthy subject; and (d) if the patient has the at least one of the high level or activity of the T cells systemically as compared to the reference sample, then administering a cancer therapy to the patient that comprises a modified dosage or administration of a Phosphoinositide 3-kinase (PI3K) inhibitor.

Abstract: Methods of treating viral diseases are disclosed herein. Certain methods include diagnostic methods that quantify levels of biological features associated with TFH or CD4-CTL cells. Certain methods include treatment methods that affect the number, functionality, activity, or expression of TFH or CD4-CTL cells or TREG cells.

Abstract: The present invention includes engineered T cell receptor (TCR) proteins, nucleic acids, vectors, host cells, methods of treating cancer, and chimeric antigen receptor expressing T cell (CAR-T) comprising an alpha chain CDR3 having the amino acid sequence of SEQ ID NO: 1, 3, 5, 7, 9, 11, 13, 15, 17, 19, 21, or 23 and/or a beta chain CDR3 having the amino acid sequence of SEQ ID NO: 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, or 24, wherein the TCR is specific for a KRAS G12>V mutation peptide, antigen-MHC binding portions, and full length portions of the same.

Abstract: Global transcriptional profiling of CTLs in tumors and adjacent non-tumor tissue from treatment-naïve patients with early stage lung cancer revealed molecular features associated with robustness of anti-tumor immune responses. Major differences in the transcriptional program of tumor-infiltrating CTLs were observed that are shared across tumor subtypes. Pathway analysis revealed enrichment of genes in cell cycle, T cell receptor (TCR) activation and co-stimulation pathways, indicating tumor-driven expansion of presumed tumor antigen-specific CTLs. Marked heterogeneity in the expression of molecules associated with TCR activation and immune checkpoints such as 4-1BB, PD1, TIM3, was also observed and their expression was positively correlated with the density of tumor-infiltrating CTLs.

Abstract: Disclosed herein are methods of detecting an antigen-specific T cell (e.g., a HDM-reactive T cell) expressing IL-9 which contribute to a worsening of an allergy (e.g., a HDM-induced allergy) or detecting an antigen-specific T cell (e.g., a HDM-reactive T cell) associated with a positive prognosis. In some embodiments, also disclosed herein is a method of treating an allergy (e.g., a HDM-induced allergy) in a subject in need thereof based on the presence or absence of an antigen-specific T cell (e.g., a HDM-reactive T cell) that express IL-9.

Abstract: The present invention includes methods of detecting follicular regulatory T cells (TFR) comprising: obtaining a biological sample from a subject and detecting whether TFR are increased in the tumor sample by contacting the biological sample with antibodies that detect CD3+CD4+ FOXP3+BCL6+ T cells CD3+CD4+CXCR5+GITR+ T cells, or both, when compared to a healthy subject, and detecting the increase of TFR in the tumor sample. The present invention also includes combination therapy that depletes follicular regulatory T cells (TFR) with minimal effect on regulatory T cells (TREGS) to prevent or reduce immune related adverse effects (irAEs).

Abstract: Disclosed herein are isolated follicular helper T cell (TFH) and engineered follicular helper T cell (TFH) and methods of isolating or engineering such cells. Further disclosed herein are methods of using such cells for treating diseases, such as cancer.

Abstract: This disclosure provides methods of treating cancer or eliciting an anti-tumor response in a subject by administering an effective amount of a population of T-cells that exhibits higher or lower than baseline expression of one or more genes. In other aspects, methods are provided to diagnose cancer and determine prognosis of cancer patients. Also provided are methods to identify the antigens or antigen receptors associated with the isolated and/or purified cell populations that elicit a more positive prognosis.

Abstract: Global transcriptional profiling of CTLs in tumors and adjacent non-tumor tissue from treatment-naive patients with early stage lung cancer revealed molecular features associated with robustness of anti-tumor immune responses. Major differences in the transcriptional program of tumor-infiltrating CTLs were observed that are shared across tumor subtypes. Pathway analysis revealed enrichment of genes in cell cycle, T cell receptor (TCR) activation and co-stimulation pathways, indicating tumor-driven expansion of presumed tumor antigen-specific CTLs. Marked heterogeneity in the expression of molecules associated with TCR activation and immune checkpoints such as 4-1BB, PD1, TIM3, was also observed and their expression was positively correlated with the density of tumor-infiltrating CTLs.

Abstract: The invention relates to novel targets for immune response modulation, treatment of tuberculosis infection and epitopes of Mycobacterium tuberculosis, or subsequences, portions or modifications thereof, and methods and compounds for treatment and prevention of tuberculosis infection.

Abstract: The invention relates to novel targets for immune response modulation, treatment of tuberculosis infection and epitopes of Mycobacterium tuberculosis, or subsequences, portions or modifications thereof, and methods and compounds for treatment and prevention of tuberculosis infection.