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1.
Viral hepatitis reactivation has been widely reported in patients undergoing immunosuppressive therapy; however, few data are available about the risk of HBV and HCV reactivation in patients with inflammatory bowel disease, receiving immunosuppressive drugs. The aim of our study was to assess the prevalence of HBV and HCV infection in a consecutive series of patients with inflammatory bowel disease and to value the effects of immunosuppressive therapy during the course of the infection. Retrospective observational multicenter study included all consecutive patients with inflammatory bowel disease who have attended seven Italian tertiary referral hospitals in the last decade. A total of 5096 patients were consecutively included: 2485 Crohn's disease and 2611 Ulcerative Colitis. 30.5% and 29.7% of the patients were investigated for HBV and HCV infection. A total of 30 HBsAg positive, 17 isolated anti‐HBc and 60 anti‐HCV‐positive patients were identified. In all, 20 patients with HBV or HCV infection received immunosuppressive therapy (six HBsAg+; four isolated anti‐HBc+ and 10 anti‐HCV+). One of six patients showed HBsAg+ and one of four isolated anti‐HBc+ experienced reactivation of hepatitis. Two of six HBsAg patients received prophylactic therapy with lamivudine. Only one of 10 anti‐HCV+ patients showed mild increase in viral load and ALT elevation. Screening procedures for HBV and HCV infection at diagnosis have been underused in patients with inflammatory bowel disease. We confirm the role of immunosuppressive therapy in HBV reactivation, but the impact on clinical course seems to be less relevant than previous reported.  相似文献   

2.
Asthma is a chronic airway inflammatory disease characterized by intense leukocyte and eosinophilic infiltration accompanied by mucus hypersecretion and tissue hyperresponsiveness. Recent evidence suggests that T‐helper (Th)2 cells and their cytokine products orchestrate the pathology of asthma. In addition, Th17 cells are implicated in the pathogenesis of antigen‐induced airway inflammation. The Th17 related cytokine interleukin (IL)‐23 plays important roles in many immunological diseases, such as experimental autoimmune encephalomyelitis, rheumatoid arthritis, psoriasis and inflammatory bowel disease. Several reports describe the role of IL‐23 in the pathogenesis of allergic asthma in both human and mice. IL‐23 leads to neutrophil infiltration in the airway of asthmatic mice, which is characteristic of severe asthma resulting from Th17 development and subsequently IL‐17 secretion. IL‐23 can also promote eosinophil infiltration in the airway, which is a hallmark of allergic asthma. These studies suggest that IL‐23 could be a promoting factor in the development of allergic asthma and likewise would be a target for asthma therapy. In support of this view, trials of anti‐IL‐23 therapy have been attempted in human and mouse asthma models with encouraging outcomes. This review presents the role of IL‐23 in asthma according to recent clinical trials and animal model studies. The proposed mechanisms of IL‐23‐induced airway inflammation and the agents currently being tested that target IL‐23 related pathways are discussed.  相似文献   

3.
Anti‐tumor necrosis factor (TNF)‐α agents emerge as the hot spot in the last decade for treating patients with inflammatory bowel disease (IBD). The effect of anti‐TNF‐α agents is satisfactory; however, some patients fail to achieve clinical response. Fortunately, in recent years, great efforts have been made and multiple novel therapies have been developed in the treatment for IBD. In this article, we aim to introduce anti‐TNF‐α drugs as well as other novel treatments currently undergoing clinical trials for IBD.  相似文献   

4.
Abstract: The immunological and genetic pathogeneses of inflammatory bowel disease (IBD) have been well elucidated in the recent years. The pharmacologic treatment of IBDs accordingly becomes to focus upon the individual pathologic step (targeting therapy), whereas the therapeutic action is not yet a pinpoint one. It has been known recently that new drugs such as biological immunomodulating agents and anti‐inflammatory cytokines have better short‐term effects in some respects than the conventional drugs, and they might alter the treatment strategy of IBDs in the near future. The limitation of pharmacologic treatments mainly results from adverse effects of the drugs, i.e. infection susceptibility, oncogenesis, teratogenesis and so forth. The extracorporeal therapy such as leukocytapheresis and photopheresis is reportedly effective for IBDs probably through immunomodulation such as decrease in circulating activated T‐lymphocytes and activated granulocytes that play a central role in the pathogenesis of IBD. It can be said that these extracorporeal treatment methods have advantage of rapid action and lack of serious adverse effects to drug therapy.  相似文献   

5.
Interleukin (IL)‐10 is an anti‐inflammatory cytokine mainly produced by monocytes and is essential for the induction of anti‐inflammatory intestinal macrophages with macrophage colony‐stimulating factor (M‐CSF). Thus, IL‐10‐ and M‐CSF‐rich conditions in colonic tissues seem to contribute to the improvement of pathological conditions in patients with inflammatory bowel diseases (IBD). We have already reported that ulinastatin, a serine protease inhibitor, increases M‐CSF production during granulocyte/monocyte (GM) adsorption to cellulose acetate (CA) beads (carriers for Adacolumn therapy). However, the effects of ulinastatin on IL‐10 production have not been clarified. The aim of the present study was to clarify the effects of ulinastatin on IL‐10 production during GM adsorption by in vitro experiments. Peripheral blood was divided into four groups: (Control) no ulinastatin added, no contact with CA beads; (1) no ulinastatin added, contact with CA beads; (2) ulinastatin added, no contact with CA beads; and (3) ulinastatin added, contact with CA beads. After incubation, IL‐10 in the plasma was measured. Compared with the level in the Control group, plasma IL‐10 was significantly higher only in group 3, in which ulinastatin was added in the presence of CA beads, but did not increase in the absence of CA beads. These results suggest that ulinastatin synergistically increases IL‐10 production with monocyte adsorption stimuli. By increasing not only M‐CSF but also IL‐10, a combination of ulinastatin and Adacolumn therapy may improve clinical efficacy for the treatment of IBD in terms of the induction of anti‐inflammatory intestinal macrophages.  相似文献   

6.
Background and Aims: The pathogenesis of enteropathy induced by non‐steroidal anti‐inflammatory drugs (NSAIDs) is still unclear, and there are no established treatments. Interleukin‐17A (IL‐17A) is a pro‐inflammatory cytokine that has been associated with the development of chronic inflammatory diseases, including autoimmune diseases. To define the role of IL‐17A in small intestinal injury and inflammation, we studied the effects of indomethacin administration in mice with targeted deletions of the IL‐17A gene. Methods: Male C57BL/6 (wild‐type) and homozygous IL‐17A‐/‐ C57BL/6 mice were subjected to this study. Indomethacin (10 mg/kg) was subcutaneously administered to induce small‐intestinal damage. Indomethacin‐induced lesions in the small intestine were evaluated by measuring the injured area and by histopathology. Also assessed were myeloperoxidase (MPO) activity, as an index of neutrophil accumulation, and intestinal mRNA expression for inflammatory cytokines. Results: The area of macroscopic ulcerative lesions, the MPO activity and the mRNA expression of inflammatory‐associated chemokines, such as keratinocyte chemoattractant (KC), monocyte chemotactic protein‐1 (MCP‐1), and granulocyte‐colony stimulating factor (G‐CSF), were significantly increased in indomethacin‐treated groups compared with the sham groups. The development of intestinal lesions by indomethacin was inhibited in IL‐17A‐/‐ mice compared with wild‐type mice, together with significant suppression of the increased levels of MPO activities and KC, MCP‐1, and G‐CSF levels. Conclusion: These findings demonstrate that IL‐17A contributes to the development of indomethacin‐induced small intestinal injury through upregulation of G‐CSF, KC, and MCP‐1. IL‐17A might be a promising new therapeutic target to treat NSAID‐induced enteritis.  相似文献   

7.
The introduction of targeted biological therapies has revolutionised the management of immune‐mediated inflammatory diseases (IMIDs) such as rheumatoid arthritis, ankylosing spondylitis, psoriasis and inflammatory bowel disease. Following treatment with these therapies, many patients experience significant improvements in different aspects of their disease, including symptoms, work productivity and other outcomes relevant for individuals and society. However, due to the complexity of biological drug development and manufacturing processes, the costs of these therapies are relatively high. Indeed, the financial burden on healthcare systems due to biological therapies is considerable and lack of patient access to effective treatment remains a concern in many parts of the world. As many reference biological therapies have now reached or are near to patent expiry, a number of ‘biosimilar’ drugs have been developed for use in various clinical settings, and some of these drugs are already in use in several countries. While the potential pharmacoeconomic benefits of cost‐effective biosimilars seem clear, several issues have been raised regarding, for example, the definition of biosimilarity and the validity of indication extrapolation, as well as the ‘switchability’ and relative immunogenicity of biosimilars and their reference drugs. In this review, these issues will be discussed with reference to CT‐P13, a biosimilar of the anti‐tumour necrosis factor monoclonal antibody infliximab, which is approved in Europe and elsewhere for the treatment of various IMIDs. Other important issues, including those related to data collection during nonclinical and clinical development of biosimilars, are also discussed.  相似文献   

8.
Crohn's disease and ulcerative colitis are chronic inflammatory disorders of the gastrointestinal tract and are collectively referred to as inflammatory bowel disease (IBD). IBD is a major cause of lifetime morbidity, has a severe impact on quality of life of patients (equivalent to that of rheumatoid arthritis, asthma, migraine or diabetes) and constitutes a substantial economic burden to the healthcare system. The introduction of anti‐tumour necrosis factor (TNF) antibodies has dramatically improved the treatment of IBD, but approximately one‐third of patients are nonresponders and another 30–50% will eventually lose the therapeutic effect or become intolerant to these antibodies. Thus, there is an urgent and unmet need for new therapies. The aetiologies of the different forms of IBD have not been fully elucidated but there is strong evidence implicating T cells and T‐cell migration to the gut in initiating and perpetuating the intestinal inflammatory process and tissue destruction. In recent years, progress in basic science has shed light on the mechanisms regulating T‐cell migration to the gut and new therapeutics targeting these pathways have been developed. It is interesting that some of the factors directing the localization of T cells to the gut have been shown to be relatively organ specific, potentially enabling new T‐cell‐targeted treatments to demonstrate improved safety whilst preserving therapeutic efficacy. Here, fundamental aspects of the gut immune system, the generation of tissue‐tropic effector T cells and the mechanisms of T‐cell trafficking to the gut mucosa will be reviewed. In addition, the role of these processes in IBD and how they have been exploited for the development of novel therapies for IBD will be discussed.  相似文献   

9.
Aims: The aim of this study was to investigate the prevalence of chronic kidney disease (CKD) among comparable patients with rheumatoid arthritis (RA) and seronegative inflammatory arthritis, and to explore any predictive factors for renal impairment. Methods: Consecutive patients with peripheral joint disease (oligo and polyarthritis) were recruited from our inflammatory arthritis clinics. We divided patients in two groups: RA group and seronegative inflammatory arthritis group. The cohort consisted of 183 patients (RA = 107, seronegative arthritis = 76 [psoriatic arthritis = 69, undifferentiated oligoarthritis = 7]). Estimated glomerular filtration rate (eGFR) was calculated using the established Modification of Diet in Renal Disease equation. Demographic details, disease‐specific characteristics, anti‐rheumatic drugs and the presence of cardiovascular diseases were recorded. Results: In total, 17.48% (n = 32) of the cohort had CKD. There was no statistically significant variation between the two groups as regards baseline demographics, disease characteristics, use of anti‐rheumatic drugs and the presence of individual cardiovascular diseases. We found that eGFR and the presence of CKD were similar among these groups. Among patients with CKD, 72% had undiagnosed CKD. No association of statistical significance was noted between CKD and the use of corticosteroids, disease‐modifying antirheumatic drugs and anti‐tumor necrosis factor agents. The association of cardiovascular diseases with CKD remained significant after adjusting for confounders (age, gender, duration of arthritis, high C‐reactive protein, use of anti‐rheumatic drugs). Conclusions: Patients with inflammatory arthritis are more prone to have CKD. This could have serious implications, as the majority of rheumatology patients use non‐steroidal anti‐inflammatory drugs and different immunosuppressives, such as methotrexate. No association of kidney dysfunction was noted with inflammatory disease‐specific characteristics; rather it appears to have a positive independent association with cardiovascular diseases.  相似文献   

10.
Remarkable advances have been made in the treatment of inflammatory bowel disease since the introduction of anti‐tumor necrosis factor‐α agents, especially for patients who are refractory to or cannot tolerate conventional therapies. Currently, infliximab, adalimumab, and golimumab are available in the East Asian medical market, and these agents have been shown to be effective for inducing and maintaining long‐term remission of inflammatory bowel disease. Despite their clinical benefits, anti‐tumor necrosis factor therapy can also lead to increased vulnerability to infections, development of autoimmune diseases and malignancy, and decreased immunogenicity of vaccinations. Because infectious diseases, such as tuberculosis, hepatitis, and influenza, remain major health problems in East Asia, more cautious use of biologics is needed. To further improve treatment efficacy and safety, close monitoring of inflammation, regular surveillance for malignancy, and regularly scheduled vaccinations are needed. Treatment strategies for biologics should be customized to meet the needs of different patients.  相似文献   

11.
Anti‐tumour necrosis factor (TNF) agents have demonstrated efficacy in inflammatory bowel disease (IBD). Cutaneous reactions such as new onset psoriasis or psoriasiform‐like reactions are among the most common adverse reactions. We retrospectively identified cases of anti‐TNF‐induced psoriasis or psoriasiform manifestations in IBD patients at a tertiary centre in Australia. A total of 10 (six females) of 270 (3.7%) IBD patients treated with anti‐TNF therapy developed drug‐induced psoriatic or psoriasiform‐like reactions: five patients were treated with infliximab and five with adalimumab; nine had Crohn disease. The time from initiation of anti‐TNF agent to onset of rash was 7.5 months on average. The most frequent distributions were the scalp (7/10) and extremities (6/10). Three patients discontinued anti‐TNF treatment with resolution of the rash. Topical treatment of the lesions allowed continued use of biological agent in the majority. Paradoxical psoriatic lesions are recognised adverse events associated with anti‐TNF therapy, but discontinuation of therapy due to dermatological complications is required only rarely, even in patients with psoriasiform lesions.  相似文献   

12.
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by the sequestration of various leukocyte subpopulations within both the developing pannus and synovial space. The chronic nature of this disease results in inflammation of multiple joints, with subsequent destruction of the joint cartilage and erosion of bone. Identification of T helper (Th)17 cells led to breaking the dichotomy of the Th1/Th2 axis in immunopathogenesis of autoimmune diseases such as RA, and its experimental model, collagen‐induced arthritis (CIA). Th17 cells produce cytokines, including interleukin (IL)‐17, IL‐6, IL‐21, IL‐22 and tumor necrosis factor (TNF)‐α, with pro‐inflammatory effects, which appear to have a role in immunopathogenesis of RA. Regarding the wide ranging production of pro‐inflammatory cytokines and chemokines by Th17 cells, it is expected that Th17 cell could be a potent pathogenic factor in disease immunopathophysiology. Thus the identification of effector mechanisms used by Th17 cells in induction of disease lesions may open new prospects for designing a new therapeutic strategy for treatment of RA.  相似文献   

13.
Aim: We have previously reported in mice the hepatic inflammatory in graft versus host response (GVHR) model due to the disparity of major histocompatibility complex class‐II. The regulatory T (Treg) cells have been reported to control excessive immune response and prevent immune‐related diseases. This study aimed to investigate the pathogenesis profiles of chronic GVHR progression, focusing on the Treg cells. Methods: GVHR mice induced by parental spleen CD4+ T cell injection were sacrificed after 0, 2, 4, and 8 weeks (G0, G2, G4, G8). Further, one GVHR group received anti‐IL‐10 antibody in advance and were maintained for 2 weeks. Pathologic profiles of hepatic infiltrating inflammatory cells were evaluated by haematoxylin and eosin and immunohistochemistry staining with surface markers including Treg cell markers. Results: Remarkable hepatic inflammatory in G2 significantly and gradually improved over time up to G8. In immunohistochemical staining, the increased IL‐10 receptor β+ Tr1 cells in G2 were maintained through to G8; although other inflammatory cells decreased from G2 to G8. By contrast, in the anti‐IL‐10 antibody received‐GVHR mice, the Tr1 cells were not detectable with significant inflammatory aggravation, while FoxP3+ Treg cells significantly enhanced. Conclusions: These findings in the GVHR mice suggest that the expression and activity of Treg cells, especially the Tr1 cells, might be key factors for pathologic alteration in immune‐related liver disease.  相似文献   

14.
Rheumatoid arthritis (RA) and periodontal disease (PD) are chronic inflammatory diseases that share similar osteoclasia, human leukocyte antigen‐DR4 allelic genes and immunological profile, and characteristic cytokines. Smoking can contribute to more severe RA and PD; secretion of pro‐inflammatory mediators destroys the soft synovial membrane and periodontium, respectively. Anti‐citrullinated protein antibodies and anti‐α‐enolase antibody are characteristic of these two diseases. Some studies suggest that PD may be associated with RA. Anti‐Porphyromonas gingivalis (P. gingivalis) antibody, but no P. gingivalis bacterium can be detected in RA patients’ joint fluid. Anti‐P. gingivalis antibody has been seen as a biomarker of RA. Both diseases share some nosogenesis and common pathological pathways. However, there are differing views on the connection between the two diseases. Interferon‐inducible‐16 (IFI16) is a genic marker of RA; moreover, the association between IFI16 and PD is rare. Some studies suggest PD is related to periodontal parameters and patient's pathological status rather than RA. Disease frequency in men and women differ between these two diseases. The expression of interleukin‐17 (IL‐17) receptor only associates with different genders in PD (PD of different sexes have different IL‐17 expressions). Periodontal local treatment only affects clinical periodontal status, and it does not alter circulating levels of IL‐6, tumor necrosis factor‐alpha or C‐reactive protein which are associated with RA. This review examines the similarities and differences between these two diseases and explores possible interactions. Importantly, we will discuss whether PD is a feature of RA and whether this knowledge provides helpful information in future treatment of both diseases.  相似文献   

15.
The etiopathology of inflammatory bowel disease (IBD) remains elusive. Accumulating evidence suggests that the abnormality of innate and adaptive immunity responses plays an important role in intestinal inflammation. IBD including Crohn's disease (CD) and ulcerative colitis (UC) is a chronic inflammatory disease of the gastrointestinal tract, which is implicated in an inappropriate and overactive mucosal immune response to luminal flora. Traditionally, CD is regarded as a Th1mediated inflammatory disorder while UC is regarded as a Th2like disease. Recently, Th17 cells were identified as a new subset of T helper cells unrelated to Th1 or Th2 cells, and several cytokines [e.g. interleukin (IL)-21, IL-23] are involved in regulating their activation and differentiation. They not only play an important role in host defense against extracellular pathogens, but are also associated with the development of autoimmunity and inflammatory response such as IBD. The identification of Th17 cells helps us to explain some of the anomalies seen in the Th1/Th2 axis and has broadened our understanding of the immunopathological effects of Th17 cells in the development of IBD.  相似文献   

16.
Inflammatory bowel disease (IBD), that is Crohn's disease (CD) and ulcerative colitis, affects about 1.5 million persons in the USA and 2.2 million in Europe. The pathophysiology of IBD involves immunological, genetic and environmental factors. The treatment is medico‐surgical but suspensive. Anti‐TNFα agents have revolutionized the treatment of IBD but have side effects. In addition, a non‐negligible percentage of patients with IBD stop or take episodically their treatment. Consequently, a nondrug therapy targeting TNFα through a physiological pathway, devoid of major side effects and with a good cost‐effectiveness ratio, would be of interest. The vagus nerve has dual anti‐inflammatory properties through its afferent (i.e. hypothalamic–pituitary–adrenal axis) and efferent (i.e. the anti‐TNFα effect of the cholinergic anti‐inflammatory pathway) fibres. We have shown that there is an inverse relationship between vagal tone and plasma TNFα level in patients with CD, and have reported, for the first time, that chronic vagus nerve stimulation has anti‐inflammatory properties in a rat model of colitis and in a pilot study performed in seven patients with moderate CD. Two of these patients failed to improve after 3 months of vagus nerve stimulation but five were in deep remission (clinical, biological and endoscopic) at 6 months of follow‐up and vagal tone was restored. No major side effects were observed. Thus, vagus nerve stimulation provides a new therapeutic option in the treatment of CD.  相似文献   

17.

Objective

Interleukin‐17 (IL‐17) is a proinflammatory cytokine that is expressed in the synovium of rheumatoid arthritis (RA) patients. This T cell cytokine is implicated in the initiation phase of arthritis. However, the role of IL‐17 during the effector phase of arthritis has still not been identified; this was the objective of the present study.

Methods

Mice with collagen‐induced arthritis (CIA) were treated with polyclonal rabbit anti‐murine IL‐17 (anti–IL‐17) antibody–positive serum or normal rabbit serum after the first signs of arthritis. In addition, during a later stage of CIA mice were selected and treated with anti–IL‐17 antibody or control serum. Arthritis was monitored visually, and joint pathology was examined radiologically and histologically. Systemic IL‐6 levels were measured by enzyme‐linked immunosorbent assay, and local synovial IL‐1 and receptor activator of NF‐κB ligand (RANKL) expression was analyzed using specific immunohistochemistry.

Results

Treatment with a neutralizing anti–IL‐17 antibody after the onset of CIA significantly reduced the severity of CIA. Radiographic analysis revealed marked suppression of joint damage in the knee and ankle joints. Histologic analysis confirmed the suppression of joint inflammation and showed prevention of cartilage and bone destruction after anti–IL‐17 antibody therapy. Systemic IL‐6 levels were significantly reduced after anti–IL‐17 antibody treatment. Moreover, fewer IL‐1β–positive and RANKL‐positive cells were detected in the synovium after treatment with neutralizing IL‐17. Interestingly, initiation of anti–IL‐17 antibody therapy during a later stage of CIA, using mice with higher clinical arthritis scores, still significantly slowed the progression of the disease.

Conclusion

IL‐17 plays a role in early stages of arthritis, but also later during disease progression. Systemic IL‐6 was reduced and fewer synovial IL‐1–positive and RANKL‐positive cells were detected after neutralizing endogenous IL‐17 treatment, suggesting both IL‐1–dependent and IL‐1–independent mechanisms of action. Our data strongly indicate that IL‐17 neutralization could provide an additional therapeutic strategy for RA, particularly in situations in which elevated IL‐17 may attenuate the response to anti–tumor necrosis factor/anti–IL‐1 therapy.
  相似文献   

18.
The management of pain and inflammation in haemophilic arthropathy is challenging due to the lack of anti‐inflammatory analgesic agents perfectly suitable for this population. Non‐steroidal anti‐inflammatory drugs (NSAIDs) are widely used in the management of arthritis due to their analgesic and anti‐inflammatory effects. Their use in persons with haemophilia (PWH), however, is limited due to increased risk of bleeding mainly from the upper gastrointestinal (UGI) tract. Cyclooxygenase‐2 (COX‐2) selective NSAIDs which have comparable analgesic effect to traditional NSAIDs (tNSAIDs) but with less UGI bleeding have been considered to be a suitable option for treatment of haemophilic arthropathy. COX‐2 inhibitors, however, have an increased in the risk of cardiovascular (CV) disease. Although the atherosclerotic burden in PWH is similar to that in the general population, the risk of CV‐related deaths is lower. PWH have a higher risk of GI bleeding and lower risk of thrombotic disease compared to general population. Therefore, when PWH require anti‐inflammatory/analgesic agents, it seems reasonable to use lowest dose of COX‐2 inhibitors for the shortest period together with a proton pump inhibitor. Helicobacter pylori infection should be tested for and eradicated prior to starting NSAID treatment in PWH. Furthermore, regular blood pressure and renal function test monitoring is required during COX‐2 inhibitor treatment.  相似文献   

19.
Intercellular communication of immune cells is critical to elicit efficient inflammatory responses. In intestinal mucosa, imbalance in pro‐inflammatory and anti‐inflammatory mediators, especially cytokines and chemokines, characterizes the underlying immune mechanisms of inflammatory bowel disease. Exosomes, small membrane vesicles secreted into the extracellular environment, are emerging as another important intercellular messenger in immune responses. A major recent breakthrough in this field unveils the capacity of exosomes to mediate the functional transfer of genetic materials (mRNAs and miRNAs) between immune cells. RAB27A and RAB27B are two small GTPases involved in exosome secretion. With respect to intestinal mucosal immunity, increased number of RAB27A‐positive immune cells and RAB27B‐positive immune cells are demonstrated in the colonic mucosa of patients with active ulcerative colitis as compared with that of healthy controls. This indicates the important role of exosome‐mediated immune responses in the pathogenesis of inflammatory bowel disease. Here, we will discuss the immune properties of exosomes and recent advances in their function with a special focus on intestinal mucosal immunity.  相似文献   

20.
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