No Abstract available.
Hypersensitivity* ; Immunity, Innate*

Group 3 innate lymphoid cells (ILC3) are an ILC subset that is characterized by the expression of retinoic acid-related orphan nuclear receptor γt (RORγt) and interleukin 22 (IL-22). This review summarizes the role of ILC3 in coordinating innate immunity and adaptive immunity based on current research and elaborate the significance of ILC3 from the perspective of immune system evolution. In addition, based on immune-related functions, we propose a possible time when ILC3 appears in the evolution of the immune system. And then, the research limitations and prospects are discussed.
Immunity, Innate ; Lymphocytes ; Tretinoin

Cell-mediated immune response is an important part of machinery in maintaining the body's homeostasis. After the innate immune system selectively activates the adaptive immune system, the cell-mediated immunity exerts its killing and clearance functions. Therefore, evaluating the level of cell-mediated immune response is crucial in the diagnosis and treatment of cancer, monitoring the immune status after organ transplantation, diagnosing and preventing viral diseases, and evaluating the effectiveness of vaccines and other areas. From the initial overall assessment of the immune effects in vivo to the precise detection of the number and function of multiple immune cells, the evaluation methods of cell-mediated immune response have greatly advanced. However, cell-mediated immune response involves multiple levels in the body, and it's difficult to choose the numerous detection methods available. The article systematically compares the evaluation methods of cell-mediated immune response at four different levels: the organism, the tissue and organ, the immune cells and the immune molecules, with the aim to facilitate the applications of related technologies.
Humans ; Immunity, Cellular ; Neoplasms/therapy* ; Immunity, Innate

BACKGROUND: The effects of the dietary administration of two heat-inactivated whole bacteria from the Vibrionaceae family, singly or combined, on innate immune response of the rainbow trout were studied. The two bacteria (Pdp11 and 51M6), which were obtained from the skin of rainbow trout, showed in vitro characteristics that suggested they could be considered as potential fish probiotics. METHODS: The fish were fed four different diets: control (non-supplemented), or diets supplemented with heat-inactivated bacteria at 10(8) cfu/g Pdp11, 10(8) cfu/g 51M6 or with 0.5x10(8) cfu/g Pdp11 plus 0.5x10(8) cfu/g 51M6 for 4 weeks. Six fish were sampled at weeks 1, 2, 3 and 4, and then the main humoral (natural haemolytic complement activity and serum peroxidase content) and cellular innate immune responses (leucocyte peroxidase content, phagocytosis, respiratory burst and cytotoxicity) were evaluated. RESULTS: The serum peroxidase content and the natural haemolytic complement activity increased with time, reaching the highest values in the third and fourth weeks of feeding, respectively. The phagocytic ability of specimens fed the mixture of the two inactivated bacteria was significantly higher than in the controls after 2 and 3 weeks of treatment. The same activity increased significantly in rainbow trout fed the Pdp11 diet for 2 weeks or the 51M6 diet for 3 weeks. Respiratory burst activity was unaffected by all the experimental diets at all times assayed. Cytotoxic activity had significantly increased after 3 weeks in fish fed the 51M6 diet. CONCLUSION: Our results demonstrated the usefulness of incorporating inactivated probiotic bacteria into fish diets.
Bacteria ; Complement System Proteins ; Diet ; Flow Cytometry ; Humans ; Immunity, Innate ; Oncorhynchus mykiss ; Peroxidase ; Phagocytosis ; Probiotics ; Respiratory Burst ; Skin ; Vibrionaceae

BACKGROUND: Human mannose-binding lectin (MBL) is a serum lectin taking part in the innate immunity by opsonizing various microorganisms for phagocytosis. The MBL serum concentration is affected by several single-nucleotide polymorphisms (SNPs) in the promoter region of the MBL2 gene. OBJECTIVE: The purpose of this study was to examine the relationship between MBL2 polymorphisms and atopic dermatitis (AD) susceptibility. METHODS: To examine whether the MBL2 SNPs are related to AD susceptibility, we examined 237 patients with AD and 94 controls by polymerase chain reaction (PCR)-restriction fragment length polymorphism and PCR-sequence specific primer analyses of four polymorphic loci: two (H/L and X/Y) within the promoter region and the other two (P/Q and A/B) within exon 1. MBL concentrations in the blood were estimated by ELISA. RESULTS: The prevalence of haplotype HYPB, leading to MBL deficiency, was significantly decreased in the AD patients compared to the controls (p=0.002), while the prevalence of haplotype HYPA was increased with a clear trend toward significance (p=0.056). The frequency of MBL2 LYPB/LXPA (odds ratio, 0.08; 95% confidence interval, 0.009~0.655; p=0.021) were significantly decreased in the AD patients. The blood log [total immunoglobulin E, IgE] levels of MBL2 HYPA/HYPA, HYPA/LYPA, HYPA/LYPB, HYPA/LYQA, and LYQA/LXPA haplotype pairs were significantly increased in the AD patients. CONCLUSION: The frequency of MBL2 HYPB haplotype was significantly decreased in the AD patients compared to the controls. The frequency of LYPB/LXPA had a possibly protective effect on AD. Moreover, the MBL2 HYPA haplotype pairs, which were related to higher blood total IgE levels, were possibly associated with extrinsic AD.
Dermatitis, Atopic* ; Enzyme-Linked Immunosorbent Assay ; Exons ; Haplotypes ; Humans ; Immunity, Innate ; Immunoglobulin E ; Immunoglobulins ; Mannose-Binding Lectin ; Phagocytosis ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide ; Prevalence ; Promoter Regions, Genetic

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.
Bacteria ; Defense Mechanisms ; Epithelial Cells ; Host-Pathogen Interactions ; Immune Evasion ; Immunity, Innate ; Inflammation ; Interleukin-8 ; Interleukins ; Neutrophils ; Peptides ; Periodontitis ; Phagocytosis ; Receptors, Pattern Recognition

Graft-versus-host disease (GVHD) is a serious complication of allogeneic hematopoietic cell transplantation (HCT) and this occurs as donor T lymphocytes, activated by recipient antigen presenting cells (APC), attack the host tissues or organs. This APC activation is a crucial initial step of influencing the outcome of GVHD and is mediated by innate immune signaling. Toll-like receptors (TLRs) and nucleotide binding oligomerization domain (NOD)-like receptors (NLRs) are important components of innate immunity; both families of receptors are known for sensing various microbial ligands or danger signals. Signaling through TLRs/NLRs regulate activities of APCs, through phagocytosis, cytokine and chemokine release, delivery of APCs from peripheral tissues to draining lymph nodes, and antigen presentation. Several TLRs/NLRs have been identified and their ligands and signaling pathways have been described. Recent findings suggest a significant association of TLR/NLR polymorphisms with the increased risk for severe GVHD. Therefore, these TLR/NLR pathways likely contributing to immune response for GVHD may serve as novel therapeutic targets to facilitate allograft tolerance. This review summarizes the role of TLRs/NLRs innate immune receptors and signaling in GVHD pathophysiology.
Antigen Presentation ; Antigen-Presenting Cells ; Cell Transplantation ; Graft vs Host Disease ; Humans ; Immunity, Innate ; Ligands ; Lymph Nodes ; Phagocytosis ; T-Lymphocytes ; Tissue Donors ; Toll-Like Receptors ; Transplantation Tolerance ; Transplants

Autophagy is a self-degradative process that removes misfolded or aggregated proteins, clears damaged organelles, as well as eliminates intracellular pathogens playing a role in innate immunity. Mycobacterium abscessus (M. abscessus) has been reported as a causative organism in nearly 80% of the rapid growing mycobacteria (RGM) pulmonary disease. The strain exhibits two different colony types: the smooth (S) one which is considered wild-type and the rough (R) one which is the mutated strain. In accordance to the colony morphology, the S and R types display varying autophagic responses in the host cells with the R type inducing elevated autophagy compared to the S type. The major difference in the autophagy could be based on the bioactive molecules exposed on the surface of the S and R types. Though autophagy has a vital role to play in the clearance of intracellular pathogens, very little is known on the autophagy induced by M. abscessus. It has been known that the intracellular pathogens employ different strategies to evade the autophagic pathway and to survive within the host cells. This review summarizes the most up-to-date findings on autophagy induced by M. abscessus morphotypes and how M. abscessus evades the autophagic machinery to divide and thrive inside the host cells. In addition, the prospects of autophagic machinery in devising new anti-infective strategies against mycobacterial infection is also been discussed.
Autophagy* ; Immunity, Innate ; Lung Diseases ; Mycobacterium* ; Organelles

Autophagy is a self-degradative process that removes misfolded or aggregated proteins, clears damaged organelles, as well as eliminates intracellular pathogens playing a role in innate immunity. Mycobacterium abscessus (M. abscessus) has been reported as a causative organism in nearly 80% of the rapid growing mycobacteria (RGM) pulmonary disease. The strain exhibits two different colony types: the smooth (S) one which is considered wild-type and the rough (R) one which is the mutated strain. In accordance to the colony morphology, the S and R types display varying autophagic responses in the host cells with the R type inducing elevated autophagy compared to the S type. The major difference in the autophagy could be based on the bioactive molecules exposed on the surface of the S and R types. Though autophagy has a vital role to play in the clearance of intracellular pathogens, very little is known on the autophagy induced by M. abscessus. It has been known that the intracellular pathogens employ different strategies to evade the autophagic pathway and to survive within the host cells. This review summarizes the most up-to-date findings on autophagy induced by M. abscessus morphotypes and how M. abscessus evades the autophagic machinery to divide and thrive inside the host cells. In addition, the prospects of autophagic machinery in devising new anti-infective strategies against mycobacterial infection is also been discussed.
Autophagy* ; Immunity, Innate ; Lung Diseases ; Mycobacterium* ; Organelles

Most of perinatological phenomenona and diseases are closely related with immune reaction. Most of initial immune responses occur through innate immunity and most causes, such as mechanical damage, hypoxia, and hyperoxia, are self and microorganisms are non-self, all of which are related with immune reaction concept. However, researches on perinatology are mainly focused on specific one or two causes of perinatal diseases, so often there is limitation to understand the basic concepts and phenomenona of the perinatal diseases. Through understanding of immune reaction concept, we can apply immune reaction theory to researches in perinatology and we can understand phenomenona in perinatology through knowledge of immune reaction. Therefore it is essential to understand historical development of immunology and concept of immune reaction for researches and treatment of perinatology.
Allergy and Immunology ; Anoxia ; Hyperoxia ; Immunity, Innate ; Perinatology*