Volume 21 Issue 3, March 2020

As a female faculty member with experience at academic institutions in the United States and in China, I reflect on the challenges encountered along the way.

As scientists, we develop technical expertise and design experiments to support (or refute) our hypotheses. With experience, we appreciate that science can be conducted in a variety of ways — each with different key questions. All are critical for advancing biomedical research.

Men have a role to play as well in leveling the playing field for women scientists. This includes creating inclusive environments and accepting women as equal partners in the pursuit of science.

The greatest discoveries in science often come from unexpected findings based on curiosity and passion, rather than a precise plan. The same is true of our careers.

Male immunologists are scientists and nothing more; female immunologists are scientists and nothing less.

Ann Ager is chair of its Forum and a trustee for the British Society for Immunology, and council member of the International Union of Immunological Societies. She discusses her role as an advocate for immunology to governments and other policy makers.

“Whatever mourns… / Whatever shares / The eternal reciprocity of tears.” —Wilfred Owen

Chronic inflammation associated with HIV-1 infection disrupts the homeostasis of gut-resident innate lymphoid cells and induces the generation and expansion of adaptive NK cells expressing TCF7, a transcription factor that sustains their effector functions and memory-like properties.

Oxidative stress in the tumor microenvironment activates expression of the phosphatase PAC1 in infiltrated T lymphocytes. PAC1 regulates the epigenetic modulator NuRD to limit the chromatin accessibility of T cell effector function genes, thereby fostering T cell exhaustion.

Highly proliferative cells have classically been thought to rely on anaerobic glycolysis for fuel. Weisel et al. show that germinal center B cells break this rule, as they primarily utilize fatty acid oxidation to meet their metabolic demands.

Regulatory T (T_reg) cells suppress antitumor immunity, but T_reg cell inhibition has been hampered by a lack of specific targets. CD36 expression by tumor-infiltrating T_reg cells may provide a way to specifically target T_reg cells in tumors.

Schwartzberg and colleagues discuss the advances and challenges for female scientists working in the field of immunology at the US NIH.

Grosschedl and colleagues identify a role for the transcription factor EBF1 in bone marrow stromal cells that is required to maintain the niche to support hematopoietic stem cells and hematopoiesis.

HIV-1 infection is associated with persistent inflammation that can contribute to a variety of comorbidities. Luban and colleagues demonstrate that HIV-1 infection results in permanent depletion of innate lymphoid cells, leading to breakdown of gut barrier function and a feed-forward inflammation loop, which includes skewing of NK cells toward an inflammatory/memory phenotype.

Yin and colleagues show that the phosphatase PAC1 (DUSP2) acts as a checkpoint in cytotoxic T cells to restrain their antitumor function.

Tumor environments are highly acidic due to high concentrations of lactic acid. Ho and colleagues report that tumor-infiltrating regulatory T cells adapt to this tumor environment by upregulating expression of CD36, which allows them to use fatty acids to fuel their metabolism.

Kohlmeier and colleagues showed that the airway environment drove transcriptional and epigenetic changes that regulated the cytolytic functions of airway T_RM cells and promoted their apoptosis due to amino acid starvation and activation of the integrated stress response.

Iannacone and colleagues show that the spatiotemporal regulation of type I interferon expression shapes the differentiation of antiviral CD4⁺ T cells into T_FH or T_H1 cells.

Germinal center B cells can undergo rapid proliferation. Shlomchik and colleagues show that germinal center B cells, unlike other rapidly proliferating cells, do not depend on glycolysis, but rather increase their peroxisome content and rewire their cellular metabolism to exclusively utilize fatty acid oxidation for their energetic needs.

The gut microbiota and their proximate immune cells engage in a dialog of reciprocal regulation. James and colleagues describe how immune cell and microbiotal populations vary along the length of the human colon.