Methods for monitoring whether a subject will be sensitive or resistant to treatment with an anti-SMAD7 therapy are disclosed. The methods are based on the determining of the amount of CCR9+ FOXP3+ T cells, CCR9+ IFN-gamma+ T cells, CCR9+ IL17A+ T cells, FOXP3+ T cells, IFN-gamma+ T cells, and/or IL17A+ T cells in a sample from the subject. Measurement of T cell populations may be determined by flow cytometry, immunohistochemistry, and/or ELISA.

The invention relates to panels of biomarkers for diagnosing and/or monitoring the progression of an active mycobacterial infection or for diagnosing the absence of a mycobacterial infection, particularly tuberculosis. Such diagnosis and/or monitoring may be differential diagnosis between active tuberculosis patients and patients with latent, non-progressing tuberculosis or healthy or sick patients, irrespective of whether the patients have been characterised as being sputum smear positive or sputum smear negative, and/or irrespective of whether they have been characterised as being HIV positive or HIV negative. The above pertain in all aspects both to pulmonary and extra pulmonary Mycobacterium tuberculosis infections, with Mycobacterium tuberculosis being the causative organism in tuberculosis.

The present invention relates to combination therapies useful for the treatment of cancer. In particular, the invention relates to a therapeutic combination which comprises a PD-1 antagonist, an ATR inhibitor and a platinating agent.

The present invention relates to Mycobacterium tuberculosis (M tuberculosis) proteins and immunologically active fragments (peptides or mimotope peptides) thereof. In particular, the invention relates to a group of M. tuberculosis proteins and peptides thereof that are both highly antigenic and characteristic of clinical strains of M. tuberculosis. Accordingly, the further relates to the use of these M. tuberculosis proteins or peptides in diagnosing, treating or preventing M. tuberculosis complex infection.

The present invention provides a method for enhancing immune cell function by activating various immune cells ex vivo and provides immune cells with enhanced function. The invention further provides an immune-related cell multifunctionality evaluation method. A biguanide antidiabetic drug selected from metformin, phenformin, and buformin is capable of enhancing immune cell multifunctionality by increasing CD8+T cells having a high ability to produce IL-2, INFα, and IFNγ. The immune-related cell multifunctionality may be evaluated by comparing immune cells treated with a biguanide antidiabetic drug selected from metformin, phenformin, and buformin, with control immune cells untreated with the biguanide antidiabetic drug. When the multifunctionality of immune cells treated with the biguanide antidiabetic drug selected from metformin, phenformin, and buformin is determined to be significantly increased compared with the control, it can be evaluated that the sensitivity of the immune cells to the therapeutic agent is improved.

The invention relates to helminthic parasite preparations and their use for treatment or prevention of GVHD in a subject that has undergone a transplant. The invention also related to helminthic parasite preparations and their use for prevention of GVHD in a subject prior to a transplant.

Disclosed are methods of isolating a TCR having antigenic specificity for a mutated amino acid sequence encoded by a cancer-specific mutation, the method comprising: identifying one or more genes in the nucleic acid of a cancer cell of a patient, each gene containing a cancer-specific mutation that encodes a mutated amino acid sequence; inducing autologous APCs of the patient to present the mutated amino acid sequence; co-culturing autologous T cells of the patient with the autologous APCs that present the mutated amino acid sequence; selecting the autologous T cells; and isolating a nucleotide sequence that encodes the TCR from the selected autologous T cells, wherein the TCR has antigenic specificity for the mutated amino acid sequence encoded by the cancer-specific mutation. Also disclosed are related methods of preparing a population of cells, populations of cells, TCRs, pharmaceutical compositions, and methods of treating or preventing cancer.

The present invention provides methods for predicting clinical outcome from a sample of a subject having ulcerative colitis (UC), comprising determining a prognostic marker profile and classifying the subject as either a responder or a non-responder. The methods can be used to monitor and to predict the progression of UC, by determining the likelihood for UC to progress either rapidly or slowly in an individual based on the presence or level of at least one marker in a sample. The methods can also be used to predict the regression of UC, by determining the likelihood for UC to regress either rapidly or slowly in an individual.

The disclosure provides methods for selecting patient sub-populations, or subjects, with inflammatory conditions such as inflammatory bowel diseases that are amenable to treatment with anti-Interleukin-23 therapy by measuring the serum levels of Interleukin-22 Binding Protein and/or the serum levels of Interferon-γ. In addition, the methods are useful in identifying sub-populations of patients with inflammatory disorders, such as psoriasis, psoriatic arthritis, rheumatoid arthritis, ankylosing spondylitis that are amenable to treatment with an anti-IL-23 therapy and/or an anti-IFN-γ therapy.

The methods, processes, and systems described herein include identifying an epitope of a peptide that may elicit an immune response in a subject. Often the methods, systems and processes may include designing and producing a composition comprising an epitope of a peptide identified using the methods or processes described herein.