Research Progress on Effects of Regulatory B Cells in Infection Immunity

B cells play immunomodulatory roles mainly by presenting antigens and producing antibodies. In recent years, some B cells were shown to exhibit regulatory functions. This type of B cell was named regulatory B cells(Bregs). Bregs can mediate immune tolerance to inhibit excessive inflammatory responses and to accelerate recovery of infl ammation by producing interleukin 10 and/or transforming growth factor β1 and other inhibitory cytokines. Studies showed that Bregs play important roles in parasites, bacteria, and viral infections. This study reviews biological characteristics, functions, and microsignal regulation of Bregs and their mechanism in infectious diseases and related research progress.

Immune Control Strategies for Vaccinia Virus-related Laboratory-acquired Infections

While presenting biological characteristics of vaccinia virus and laboratory-acquired infections during related research processes, this paper focuses on benefits and risks of vaccinia virus immunization in relation to laboratory-acquired infections, describes characteristics and the adaptation of vaccinia virus vaccine, analyses the role vaccinia virus immunization plays in the prevention and control of laboratory-acquired infections, and finally proposes solutions and countermeasures to further promote and implement immune control strategies. The problem related to immune strategy and laboratory- acquired infections which is being raised, analyzed and explored plays an active and instructive role in vaccinia virus related researches and laboratory- acquired infections, and also helps to recommend and develop relevant immune strategy for future vaccine control of such infections.

Viruses and autism: A Bi-mutual cause and effect

Autism spectrum disorder(ASD)is a group of heterogeneous,multi-factorial,neurodevelopmental disorders resulting from genetic and environmental factors interplay.Infection is a significant trigger of autism,especially during the critical developmental period.There is a strong interplay between the viral infection as a trigger and a result of ASD.We aim to highlight the mutual relationship between autism and viruses.We performed a thorough literature review and included 158 research in this review.Most of the literature agreed on the possible effects of the viral infection during the critical period of development on the risk of developing autism,especially for specific viral infections such as Rubella,Cytomegalovirus,Herpes Simplex virus,Varicella Zoster Virus,Influenza virus,Zika virus,and severe acute respiratory syndrome coronavirus 2.Viral infection directly infects the brain,triggers immune activation,induces epigenetic changes,and raises the risks of having a child with autism.At the same time,there is some evidence of increased risk of infection,including viral infections in children with autism,due to lots of factors.There is an increased risk of developing autism with a specific viral infection during the early developmental period and an increased risk of viral infections in children with autism.In addition,children with autism are at increased risk of infection,including viruses.Every effort should be made to prevent maternal and early-life infections and reduce the risk of autism.Immune modulation of children with autism should be considered to reduce the risk of infection.

Type I strain of Toxoplasma gondii from chicken induced different immune responses with that from human,cat and swine in chicken

In this study,four strains of Toxoplasma gondii with the same genetic type（Type I） originated from chicken,human,cat and swine were used to compare the immune responses in resistant chicken host to investigate the relationships between the parasite origins and the pathogenicity in certain host.A total of 300,10-day-old chickens were allocated randomly into five groups which named JS（from chicken）,CAT（from cat）,CN（from swine）,RH（from human） and a negative control group（—Ve） with 60 birds in each group.Tachyzoites of four different T.gondii strains（JS,CAT,CN and RH） were inoculated intraperitoneally with the dose of 1×10~7 in the four designed groups,respectively.The negative control（-Ve） group was mockly inoculated with phosphate-buffered saline（PBS） alone.Blood and spleen samples were obtained on the day of inoculation（day 0） and at days 4,11,25,39 and 53 post-infection to screen the immunopathological changes.The results demonstrated some different immune characters of T.gondii infected chickens with that of mice or swine previous reported.These differences included up-regulation of major histocompatibility complex class Ⅱ（MHC Ⅱ） molecules in the early stage of infection,early peak expressions of interleukin（IL）-12（IL-12） and-10（IL-10） and long keep of IL-17.These might partially contribute to the resistance of chicken to T.gondii infection.Comparisons to chickens infected with strains from human,cat and swine,chickens infected with strain from chicken showed significant high levels of CD4~＋ and CD8~＋ T cells,interferon gamma（IFN-γ）,IL-12 and IL-10.It suggested that the strain from chicken had different ability to stimulate cellular immunity in chicken.

Congenital infection of rabbits with Schistosoma japonicum and protective immunity of offspring

Background Recently congenital infection with Schistosoma japonicum (S. japonicum) has been domonstrated in pigs, rabbits, mice and dogs. We explored the rabbit as an animal model for the congenital infection of schistosomiasis japonica and assessed the effect of a congenital S. japonicum infection on the resistance of rabbit kittens to a postnatal challenge infection.Methods Sixteen pregnant New Zealand white rabbits were infected with a single dose of S. japonicum cercariae. The exposed animals were divided into three groups according to the gestation age at the time of infection. Diagnosis of prenatally acquired S. japonicum infection in the rabbit kittens was primarily based on serological tests in combination with parasitological and histopathological findings. Congenitally infected kittens were challenged percutaneously with 100 S. japonicum cercariae to assess the effect of a congenital S. japonicum infection on kitten resistance to a postnatal challenge infection.Results The overall prevalence of congenital infection in offspring of infected mothers was 20% (12/60). The congenital infection rate in group L (late gestation) was much higher than in group E (early gestation) and group M (mid-gestation) (P<0.05). After a postnatal challenge infection, prenatally infected kittens had a 54.66% worm reduction rate, 41.45% egg reduction rate, and 51.76% granuloma size reduction rate compared to nave kittens.Conclusions This study demonstrates the possibility of congenital infection of S. japonicum in rabbits and the resistance of congenitally infected kittens to a postnatal challenge infection. These results have important implications not only for epidemiological investigations, but also in designing government control programs for schistosomiasis.

Immunological changes of chicken infected with marek's disease virus

The experiment was conducted to infect one-day old healthy AA chicks with virulent Marek'sdisease virus(MDV).Compared with the uninfected control chicks,it was undertaken to detect theinductive activity of interlukin-2,expression of IL-2 recepter(IL-2R)and proliferative reaction ofT cell in the thymus and spleen;to determine the number of α-naphthyl esterase positive T cells,acid phosphatase positive T cells and antibody forming cells in the thymus,Bursa Fabricius,spleen,cecal tonsil, Harder gland and mucosal lympoid tissue of bronchus;to check the number of T cell inperipheral blood as well as the dynamic changes of the amount of IgG, IgM and IgA in the serum,tear, trachea washings and intestinal secretions of infected chickens at 5,25,45 days old,respectively.The experimental results reveal that immunoregulation of IL-2 in immune organs ofinfected chickens was disordered;the cellular and humoral immune functions weresignificantly depressed in the central and peripheral immune organs;the local or mucosal immunedefense function were also markedly decreased in respiratory and digestive tracts.

Senescent remodeling of the immune system and its contribution to the predisposition of the elderly to infections

Objective To review the senescent remodeling of the immune system with aging and its relevance to the increased susceptibility of the elderly to infectious diseases, along with an outlook on emerging immunological biomarkers. Data sources The data selected were from PubMed with relevant published articles in English or French from 1995 to the present. Searches were made using the terms immunosenescence and aging paired with the following： innate immunity, T-celr, B-cell, adaptive immunity and biomarkers. Articles were reviewed for additional citations and some information was gathered from web searches. Study selection Articles on aging of both the innate and adaptive immunity were reviewed, with special attention to the remodeling effect on the ability of the immune system to fight infectious diseases. Articles related to biomarkers of immunosenescence were selected with the goal of identifying immunological biomarkers predisposing the elderly to infections. Results Innate immunity is generally thought to be relatively well preserved or enhanced during aging compared with adaptive immunity which manifests more profound alterations. However, evidence, particularly in the last decade, reveals that both limbs of the immune system undergo profound remodeling with aging. Reported data on adaptive immunity is consistent and changes are well established but conflicting results about innate immunity were reported between in vivo and in vitro studies, as well as between murine and human studies. Epidemiological data suggests increased predisposition of the elderly to infections, but no compelling scientific evidence has directly linked senescent immune remodeling to this increased susceptibility. Recently, growing interest in identifying immunological biomarkers and defining immune risk phenotypes/profiles （IRP） has been expressed. Identification of biomarkers is in its early days and few potential biomarkers have been identified, with the Swedish having defined one IRP based on the adaptive immune response. Conclusions Aging does not necessarily lead to an unavoidable decline in immune functions. Instead, a complex remodeling occurs. Despite the lack of compelling scientific evidence, senescent immune remodeling surely is a significant contributing factor to the increased risk and severity of infections in the elderly. Although, no immunological biomarker has been formally linked to the increased risk of infections in the elderly, biomarkers remain a promising tool to predict the likelihood of healthy aging, the level of immune competence, and mortality risk in the elderly. Hence, more research is required to define healthy aging and identify immunological biomarkers.

Septic cardiomyopathy:characteristics,evaluation,and mechanism

Sepsis is a common clinical disease;if there is no early active treatment,it is likely to develop into multiple organ dysfunction syndrome and even cause death.Septic cardiomyopathy is a complication of sepsis-related cardiovascular failure,characterized by reversible left ventricular dilatation and decreased ventricular systolic and/or diastolic function.At present,echocardiography and biomarkers are often used to screen septic cardiomyopathy in clinics.Although there is still a lack of clear diagnostic criteria for septic cardiomyopathy,according to existing studies,the pathogenesis of several septic cardiomyopathy has been clarified,such as immune response caused by infection and mitochondrial dysfunction.This review summarizes the characteristics,pathophysiology,and diagnosis of septic cardiomyopathy and focuses on the mechanisms of infection immunity and mitochondrial dysfunction.