Allergic rhinitis (AR) is a global health problem with increasing prevalence and association with an enormous medical and socioeconomic burden. New recognition of immune cells such as type 2 innate lymphocytes (ILC2s), T helper (Th2) 2 cells, follicular helper T cells, follicular regulatory T cells, regulatory T cells, B cells, dendritic cells, and epithelial cells in AR pathogenesis has been updated in this review paper. An in‐depth understanding of the mechanisms underlying AR will aid the identification of biomarkers associated with disease and ultimately provide valuable parameters critical to guide personalized targeted therapy. As the only etiological treatment option for AR, allergen‐specific immunotherapy (AIT) has attracted increasing attention, with evidence for effectiveness of AIT recently demonstrated in several randomized controlled trials and long‐term real‐life studies. The exploration of biologics as therapeutic options has only involved anti‐IgE and anti‐type 2 inflammatory agents; however, the cost‐effectiveness of these agents remains to be elucidated precisely. In the midst of the currently on‐going COVID‐19 pandemic, a global life‐threatening disease, although some studies have indicated that AR is not a risk factor for severity and mortality of COVID‐19, this needs to be confirmed in multi‐centre, real‐life studies of AR patients from different parts of the world.

Update on pathomechanisms and treatments in allergic rhinitis

T follicular helper cells in autoimmune diseases.

Primary anti-phospholipid antibody syndrome (pAPS) is a multi-organ autoimmune disease, and autoantibodies are involved in its pathogenesis. Follicular helper T cells (Tfh) and follicular regulatory T cells (Tfr) are critical for B cell maturation and antibody production, but their roles in pAPS remain unknown. We enrolled 32 pAPS patients and 23 healthy controls (HCs) and comprehensively analyzed circulating Tfh and Tfr, as well as their subsets, using flow cytometry. Clinical data including autoantibody levels were collected and their correlations with Tfh and Tfr subsets were analyzed. In addition, correlation analyses between B cell functional subsets and Tfh and Tfr were performed. Changes and potential effects of serum cytokines on Tfr and Tfh were further explored. We found the circulating Tfr was significantly decreased while Tfh and Tfh/Tfr ratios were increased in pAPS patients. Tfh2, inducible T cell co-stimulator (ICOS)+  programmed cell death 1 (PD-1)+  Tfh and Ki-67+  Tfh percentages were elevated, while CD45RA- forkhead box protein 3 (FoxP3)hi , Helios+ , T cell immunoglobulin and ITIM (TIGIT)+  and Ki-67+  Tfr percentages were decreased in pAPS patients. New memory B cells and plasmablasts were increased and altered B cell subsets and serum autoantibodies were positively correlated with Tfh, Tfh2, ICOS+ PD-1+  Tfh cells and negatively associated with Tfr, CD45RA- FoxP3hi Tfr and Helios+  Tfr cells. In addition, pAPS with LA/aCL/β2GPI autoantibodies showed lower functional Tfr subsets and higher activated Tfh subsets. Serum interleukin (IL)-4, IL-21, IL-12 and transforming growth factor (TGF)-β1 were up-regulated and associated with Tfh and Tfr subset changes. Our study demonstrates that imbalance of circulating Tfr and Tfh, as well as their functional subsets, is associated with abnormal autoantibody levels in pAPS, which may contribute to the pathogenesis of pAPS.

Follicular Helper and Follicular Regulatory T Cell Subsets Imbalance is Associated with higher activated B cells and Abnormal Auto-antibody Production in Primary Anti-phospholipid Syndrome Patients

The MHC-self immunopeptidome of professional antigen presenting cells is a cognate ligand for the TCRs expressed on both conventional and thymic-derived natural regulatory T cells. In regulatory T cells, the TCR signaling associated with MHC-peptide recognition induces antigen specific as well as bystander immunosuppression. On the other hand, TCR activation of conventional T cells is associated with protective immunity. As such the peripheral T cell repertoire is populated by a number of T cells with different phenotypes and different TCRs, which can recognize the same MHC-self-peptide complex, resulting in opposite immunological outcomes. This article summarizes what is known about regulatory and conventional T cell recognition of the MHC-self-immunopeptidome at steady state and in inflammatory conditions associated with increased T and B cell self-reactivity, discussing how changes in the MHC-ligandome including epitope copy number and post-translational modifications can tilt the balance toward the expansion of pro-inflammatory or regulatory T cells.

/pdf/the-yin-yang-balance-of-the-mhc-self-immunopeptidome-2vb3utcr.pdf

The yin/yang balance of the MHC-self-immunopeptidome

Natural killer (NK) cells were reported to be involved in the pathogenesis of primary antiphospholipid syndrome (pAPS). Immunosuppressive receptor TIGIT and activating receptor CD226 are specifically expressed on NK cells with competitive functions. This study aims to investigate the expression diversities of CD226/TIGIT on NK subsets and their associations with NK subsets activation phenotypes and potential clinical significance, furthermore, to explore potential cause for CD226/TIGIT expression diversities in pAPS. We comparatively assessed the changes of CD56brightNK, CD56dimNK and NK-like cells in seventy pAPS patients compared with control groups, including SLE, asymptomatic-carriers of aPLs, and healthy controls (HCs) and their expression diversities of CD226/TIGIT by flow cytometry. CD25, CD69, CD107α expression and IFN-γ secretion levels of NK subsets were detected to determine the potential association of CD226/TIGIT expression with NK subsets activation. CD226/TIGIT expression levels were compared among different subgroups divided by aPLs status. Moreover, in-vitro cultures were conducted to explore the potential mechanisms of CD226/TIGIT expression imbalance. Results: CD56brightNK and CD3+CD56+NK-like cells were significantly increased while CD56dimNK cells were obviously decreased in pAPS, and CD56brightNK and NK-like cells exhibited significantly higher CD226 but lower TIGIT expressions. CD226+CD56brightNK and TIGIT-CD56brightNK cells show higher CD69 expression and IFN-γ secretion capacity, and CD226+NK-like and TIGIT-NK-like cells showed higher expressions of CD25 and CD69 but lower apoptosis than CD226- and TIGIT+CD56brightNK/NK-like cells, respectively. The imbalanced CD226/TIGIT expressions were most significant in aPLs triple-positive group. Expression imbalanced of CD226/TIGIT on CD56brightNK and NK-like cells were aggravated after IL-4 stimulation and recovered after tofacitinib blocking. Conclusion: Our data revealed significant imbalanced CD226/TIGIT expressions on NK cells in pAPS, which closely associated with activated NK subsets phenotypes and more complicated autoantibody status. CD226/TIGIT imbalanced may be affected by IL-4/JAK pathway activation.

Altered CD226/TIGIT expressions were associated with activated NK phenotypes in primary anti-phospholipid syndrome and affected by IL-4/JAK pathway.

Objective
To investigate the clinical characteristics of the human Adenovirus (HAdv) infections in allogeneic hematopoietic stem cell transplantation (allo-HSCT) patients and explore the clinical significance of HAdv monitoring.


Methods
A total of 845 cases underwent allo-HSCT were included retrospectively in Perking University People′s Hospital from October 2012 to August 2014.Peripheral blood HAdv load were monitored twice weekly within 100 days after allo-HSCT, or whenever necessary quantitatively by real-time PCR. Meanwhile, other clinical samples such as stool, urine, and bronchoalveolar lavage fluid (BLAF) were also detected qualitatively whenever necessary. The follow-up period was at least six months after allo-HSCT. All clinical data were collected and analyzed.


Results
The total positive rate of HAdv was 3.4% (29/845). The incidence of HAdv infection was higher in children [3.8% (6/155), 2) clinically, 1 cases with pneumonia. There were 8 cases of death at the end of follow-up.


Conclusions
HAdv is an important pathogen causing infection in patients after allo-HSCT. The infenction is characterized with multiple organ involvement.CMV and EBV coinfection is common. HAdv monitoring was of great significance in allo-HSCT patients.(Chin J Lab Med, 2017, 40: 133-137)


Key words: 
Adenovirus infections, human; Hematopoietic stem cell transplantation; Transplantation, allogene

Clinical characteristics of Adenovirus infections and effective monitoring in patients undergoing allogeneic hematopoietic stem cell transplantation

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Follicular Helper and Follicular Regulatory T Cell Subsets Imbalance is Associated with higher activated B cells and Abnormal Auto-antibody Production in Primary Anti-phospholipid Syndrome Patients

Clinical characteristics of Adenovirus infections and effective monitoring in patients undergoing allogeneic hematopoietic stem cell transplantation