Dysregulation of intestinal microflora is linked to inflammatory disorders associated with compromised immunosuppressive functions of Foxp3+ T regulatory (Treg) cells. Although mucosa-associated commensal microbiota has been implicated in Treg generation, molecular identities of the “effector” components controlling this process remain largely unknown. Here, we have defined Bifidobacterium bifidum as a potent inducer of Foxp3+ Treg cells with diverse T cell receptor specificity to dietary antigens, commensal bacteria, and B. bifidum itself. Cell surface β-glucan/galactan (CSGG) polysaccharides of B. bifidum were identified as key components responsible for Treg induction. CSGG efficiently recapitulated the activity of whole bacteria and acted via regulatory dendritic cells through a partially Toll-like receptor 2–mediated mechanism. Treg cells induced by B. bifidum or purified CSGG display stable and robust suppressive capacity toward experimental colitis. By identifying CSGG as a functional component of Treg-inducing bacteria, our studies highlight the immunomodulatory potential of CSGG and CSGG-producing microbes.

In BriefSingle-nucleotide polymorphisms in ETS1 are associated with systemic lupus erythematosus (SLE). Kim et al. show that Ets1 deletion in T cells, but not B cells or DCs, result in SLE-like humoral autoimmunity, which was due to the expansion of GATA-3 + Bcl6 + Tfh2 cells and could be alleviated by neutralizing IL-4. Tfh2 frequencies in SLE patients correlate with disease parameters, suggesting therapeutic relevance for IL-4 blockade.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with diverse manifestations, and its pathogenesis is unclear and complicated. Infection and SLE are similar in that they both cause inf lammatory reactions in the immune system; however, one functions to protect the body, whereas the other is activated to damage the body. Infection is known as one of the common trigger factors for SLE; there are a number of reports on infectious agents that provoke autoimmune response. Several viruses, bacteria, and protozoa were revealed to cause immune dysfunction by molecular mimicry, epitope spreading, and bystander activation. In contrast, certain pathogens were revealed to protect from immune dysregulation. Infection can be threatening to patients with SLE who have a compromised immune system, and it is regarded as one of the common causes of mortality in SLE. A clinical distinction between infection and lupus f lare up is required when patients with SLE present fevers. With a close-up assessment of symptoms and physical examination, C-reactive protein and disease activity markers play a major role in differentiating the different disease conditions. Vaccination is necessary because protection against infection is important in patients with SLE.

The KPSS-10 exhibited a first-order, two-factor construct, and excellent reliability and validity were established for Korean patients with chronic disease. The psychometric properties of the shortest version, KPSS-4, were only marginally acceptable.

Neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and platelet-to-lymphocyte ratio (PLR) have been investigated as disease activity markers for systemic lupus erythematosus (SLE). Hence, we investigated the clinical significance of these parameters in diagnosing infection in patients with SLE. In total, 120 patients with SLE, who were admitted to hospital due to disease flares or infection, were recruited for the study. Of the 120 patients, 60 had a concurrent infection (SLE with infection), while the remaining 60 patients were admitted with a flare without any evidence of infection (SLE with flare). NLR was higher in the patients with SLE with infection, compared to patients with SLE with flare (14.2 ± 15.4 versus 3.3 ± 2.2, p < 0.001). Additionally, PLR was higher in the SLE with infection group than in the SLE with flare group (357.7 ± 350.1 versus 231.7 ± 152.9, p = 0.012), but not MLR. In the SLE with infection group, C-reactive protein (CRP) levels positively correlated with NLR and PLR. NLR with a cut-off value of 5.70 and an area under the curve (AUC) of 0.872 indicated good sensitivity (75%) and specificity (90%), for the diagnosis of SLE with infection. CRP with a cut-off value of 1.28 mg/dL (AUC 0.942) showed the sensitivity (93.3%) and specificity (91.7%). NLR with a cut-off value of 5.70 and CRP with a cut-off value of 1.28 mg/dL showed the increased specificity (98.3%) than only CRP, but not significant. NLR could be a good additive marker for diagnosing infection in patients with SLE.