Humidity and immunity

Infection with respiratory viruses often
increases during the colder and less-humid
winter months; however, the host-intrinsic
factors that contribute to this enhanced
susceptibility have remained largely unclear.
Iwasaki and colleagues, in the Proceedings
of the National Academy of Sciences, report
on infection with influenza A virus in mice
kept under normal or low ambient humidity.
Infection under low-humidity conditions
results in worse symptoms, less-efficient
epithelial repair, impaired mucociliary and
innate immune cell–dependent clearance
of the virus and reduced control of viral
spreading. Furthermore, the expression
of key interferon-regulated genes is also
reduced under low relative humidity. The
mechanism that underpins these diverse
impairments seen under low humidity
remains unknown but might be related to
the induction of stress responses.

In Nature, Mempel and colleagues show
that disruption of the CARMA1–BCL10–
MALT1 signalosome complex in Treg cells
leads to production of the cytokine IFN-γ
in these cells and the initiation of tumor
control. Homozygous deletion of Carma1
in Treg cells (via Foxp3-Cre) in mice results in
Treg cell secretion of IFN-γ and multi-organ
inflammation, but heterozygous deletion
does not, whereas both homozygous tumor-
infiltrating CARMA1-deficient Treg cells
and their heterozygous counterparts secrete
IFN-γ and are sufficient to diminish tumor
growth. Acute deletion of CARMA1 in
Treg cells reduces growth in already
established tumors, and both constitutive
deletion and acute deletion of CARMA1
in Treg cells trigger expression of the
inhibitory ligand PD-L1 on tumor cells.
Inhibitors of the paracaspase activity of
MALT1 have effects similar to those of
the Treg cell deletion of CARMA1 and act
in synergy with treatment with antibody
to the inhibitory receptor PD-1 to induce
tumor control and relapse-free rejection in
checkpoint blockade–resistant tumors.

Study of human antibody responses in
patients who survived infection with EV.
Despite a robust B cell response to viral
proteins early after infection, neutralizing
anti-viral responses arose months after
infection. Similarly, somatic hypermutation
frequencies and immunoglobulin G4
responses arose much later. Analysis
of protective neutralizing monoclonal
antibodies (mAbs) reveals common EV
glycoprotein core elements that might be
targeted by vaccines. Multiple independent
clones use IGHV3-13*03 variable segments
and express a complementarity-determining
region 3 of 12 amino acids that includes
central phenylalanine–glycine residues.
Notably, in vitro screening assays with
EV glycoprotein successfully discriminate
neutralizing mAbs from non-neutralizing
mAbs, which might prove useful in
vaccine-development studies.

Source: https://www.nature.com/articles/s41590-019-0434-x#:~