Akt2 deficiency impairs Th17 differentiation, augments Th2 differentiation, and alters the peripheral response to immunization.

Akt1 and Akt2, isoforms of the serine threonine kinase Akt, are essential for T cell development. However, their role in peripheral T cell differentiation remains undefined. Using mice with germline deletions of either Akt1 or Akt2, we found that both isoforms are important for Th17 differentiation, although Akt2 loss had a greater impact than loss of Akt1.

Advancing Equity in Cancer Care: The Critical Role of Sexual Orientation and Gender Identity Data Collection.

New study highlights critical gaps and opportunities to enhance equitable cancer care for sexual and gender minority patients.

Impact of Correcting Nutritional Deficiency Anemias in the Elderly on Hospitalizations, Falls, and Mortalities.

Background: The incidence and prevalence of anemia increase with age, particularly in adults older than 65 years, and it is associated with a number of adverse health outcomes (AHO), particularly hospitalizations, falls and mortalities. Given that approximately one-third of these anemias are due to reversible causes, we studied whether the treatment of nutritional deficiency anemia (NDA), namely iron deficiency anemia (IDA), cobalamin deficiency anemia (CDA), and folate deficiency anemia (FDA), improves AHO; and explored whether each NDA had different AHO.

Methods: We reviewed electronic medical records of our internal medicine office patients aged 65 years or older, who had a diagnosis of anemia in a non-acute setting.

Association Between Obesity and Cancer Mortality: An Internal Medicine Outpatient Clinic Perspective.

Background: Obesity is one of the leading preventable causes of cancer that has a causal relationship with cancers of esophagus, breast and colon. Paradoxically, there are studies demonstrating that obesity is associated with improved survival in cancer patients. The aim of our study was to investigate the association of obesity and cancer mortality in adult patients.

Aplastic anemia in a patient with CVID due to NFKB1 haploinsufficiency.

Acquired aplastic anemia (AA) is a life-threatening bone marrow failure caused by an autoimmune cytotoxic T lymphocyte attack on hematopoietic stem and progenitor cells. Factors contributing to aberrant autoimmune activation in AA include a deficit of T regulatory cells and high levels of inflammatory cytokines. Several acquired conditions of immune dysregulation and genetic polymorphisms in inflammatory cytokines and human leukocyte antigen genes have been linked to an increased risk of AA.

mTORC2 regulates multiple aspects of NKT-cell development and function.

Invariant NKT (iNKT) cells bridge innate and adaptive immunity by rapidly secreting cytokines and lysing targets following TCR recognition of lipid antigens. Based on their ability to secrete IFN-γ, IL-4 and IL-17A, iNKT-cells are classified as NKT-1, NKT-2, and NKT-17 subsets, respectively. The molecular pathways regulating iNKT-cell fate are not fully defined.

Natural and inducible TH17 cells are regulated differently by Akt and mTOR pathways.

Natural T helper 17 (nTH17) cells are a population of interleukin 17 (IL-17)-producing cells that acquire effector function in the thymus during development. Here we demonstrate that the serine/threonine kinase Akt has a critical role in regulating nTH17 cell development. Although Akt and the downstream mTORC1-ARNT-HIFα axis were required for generation of inducible TH17 (iTH17) cells, nTH17 cells developed independently of mTORC1.