mucosal surfaces are constantly exposed to the external environment , which includes commensal microbes and exogenous antigens . when pathogenic microbes breach the surface barrier , surveillance systems beneath sense the trespassers and send an alarm to defense headquarters . mucosal immune tissues comprise lymphoid organs associated with the gastro - intestinal tract ( e.g. , intestine , oral cavity and pharynx ) , respiratory tract , and urogenital tract , as well as the glands associated with these tissues , such as the salivary glands and lacrimal glands ( 1 ) . mucosal immunity can maintain peaceful body surface by generating secretory iga ( siga ) from b cells as well as priming specific t cell immunity . the intestine , especially , harbors an enormous community of commensal microorganisms that may contribute to host defense by enforcing the host 's barrier function ( 2 ) or by competing against other microorganisms metabolically ( 3,4 ) . dendritic cells ( dcs ) or other phagocytic cells continuously survey the mucosal environment by using innate pattern recognition receptors and sample antigens prior to integrate adaptive immune system . these cells also can adjust suppressive regulation to innocuous antigens by inducing tregs and keep distance to commensals by producing siga . moreover , these cells protect against pathogenic invasion by generating various kinds of helper t ( th ) and cd8 t cells as well as helping to produce siga antibodies . here , we provide an overview of the gut immune response , focusing on unique functional features of intestinal dcs and other phagocytic cells . lamina propria dcs in the small intestine ( si ) haves been well studied as one of the intestinal dc subsets . cd11c major histocompatibility ( mhc ) class ii cells in the gut comprise dcs as well as phagocytic macrophages . genuine dcs are a cd11c mhc class ii population , whereas macrophages are a cd11c mhc class ii population ( 5 ) . lamina propria phagocytic cells in the gut have different origins and functions ( 6 ) . dc subsets are differentiated by flt3 ligand - dependent manner whereas cx3cr1-expressing phagocytic cells are dependent on csf-1r ( 6 ) . peripheral cd103cd11b dcs are developmentally dependent on batf3 and are related to cd8 conventional dcs ( 7 ) . dc migration is tightly controlled by the expression of ccr7 , and it can be largely classified as non - migratory and migratory ( 8,9 ) . . migratory dcs travel into draining lymph nodes with sampled antigen and can be infiltrated under inflammation . dc and phagocytic cells in the gut and their functions therein are listed in table i. in the gut , cd103 cd11b dcs has been well reported by the function to induce lymphocytes . gut cd103 dcs comprise two major subsets , cd103cd11b and cd103cd11b dcs ( 10 ) . cd103 cd11b dcs are the dominant population of cd103 dc in the peyer 's patches and colon lamina propria ( 11 ) . in contrast , cd103cd11b dcs are the major dc subset in the si lamina propria ( 12 ) . in addition tnf-/inos - producing dcs ( tip dcs ) were initially reported in the spleen , where they released large amounts of nitric oxide ( no ) after recognizing commensal bacteria through toll - like receptors ( tlrs ) ( 13 ) . the presentation of innocuous food antigens by antigen - presenting cells induces oral tolerance by generation of inducible regulatory t ( treg ) cells ( 14 ) . cd103cd11b dcs can sample soluble antigens from the intestinal lumen through a process termed goblet cell - associated antigen passages ( gaps ) ( 15 ) ( fig . 1 ) . these dcs can also patrol among enterocytes while extending dendrites toward the lumen ( 16 ) . these intraepithelial cd103 dcs are recruited to sample bacterial antigens for presentation . in the si lamina propria as well as mesenteric lymph node ( mln ) , these dcs express retinaldehyde dehydrogenase type 2 ( raldh2 ) which can convert retinal to retinoic acid ( ra ) , a metabolic derivative of vitamin a found in food . this dc subset can induce regulatory foxp3cd4 t cells dependent on ra and tgf- ( 17,18,19 ) ; alternatively , cd11b f4/80cd11c macrophages in the lamina propria has been reported as more potent inducers of treg cells than dcs ( 20 ) . cx3cr1 phagocytic cells in the lamina propria support expansion of the foxp3cd4 treg cell population by producing il-10 to harness immune tolerance ( 21 ) . cx3cr1 phagocytic cells can capture salmonella by extending dendrites across epithelium in a cx3cr1-dependent manner ( 22 ) . antigens captured by cx3cr1 phagocytic cells can be transferred through gap junctions to cd103 dcs in the lamina propria to establish oral tolerance ( 23 ) . in addition to luminal antigen , lamina propria cx3cr1 cells facilitate the surveillance of circulatory antigens from blood vessels ( 24 ) . these cells fail to prime nave cd4 t cells ; however , cross - presentation by these cells can induce priming of and differentiation into cd8 t cells that express il-10 , il-13 , and il-9 . these cd8 t cells can suppress pathogen - specific cd4 t cell activation through il-10 ( 24 ) . finally , these cd8 t cells act as a regulatory cd8 tcr   t cell population in the epithelium . cx3cr1 cells regulate colonic il-22 producing group 3 innate lymphoid cells ( ilc3 ) to promote mucosal healing and maintain barrier integrity ( 25 ) . therefore , cd103 dcs and cx3cr1 phagocytic cells can generate two distinct regulatory t cell subsets by different mechanisms to maintain gut immune homeostasis at steady state ( fig . 1 ) . pdcs may mediate anti - inflammatory responses following tlr2-polysaccharide a signaling ( 26 ) and type i interferon supports treg function and regulates colitis ( 27,28 ) . after dcs sample antigen in the lamina propria , they can present antigenic epitope to nave t cells in the isolated lymphoid follicles ( ilf ) or draining mln . cd103cd11b dcs , one of the major dc subset in the si lamina propria , are primarily a migratory population that responds to ccr7 expression and can be infiltrated under inflammatory conditions ( 29,30 ) . segmented filamentous bacteria ( sfb ) , murine commensal bacteria , are shown to be sufficient for th17 differentiation ( 31 ) . mhc ii - dependent presentation of sfb antigens by intestinal dcs is crucial for th17 cell induction ( 32 ) . cd103 cd11b dcs produce il-6 with tlr stimuli which enable to induce th17 cell differentiation ( 34 ) . several studies suggest the possibility that cd103cd11b dcs might interact with sfb and link signals to induce th17 . cd103 cd11b dcs can express high amounts of il-23 following tlr5 stimuli and then drove il-22-dependent regiii production from paneth cells ( 35 ) . tlr5 dcs promote the differentiation of antigen - specific th17 and th1 cells following stimulation by flagellin , a tlr5 ligand ( 36 ) . cd103cd11bcd8 dcs expressing tlr3 , tlr7 , and tlr9 can produce il-6 and il-12p40 following stimulation of the respective tlr ligands ( 37 ) . while their function under conditions of inflammation or infection remains unclear , their suppressive functions are well described at steady state . a unique feature of the mucosal immune system is local production of siga from plasma cells differentiated from b cells . iga class switching generally occurs in gut - associated lymphoid tissues including peyer 's patches , mlns , and ilfs within the lamina propria . sfb stimulates the postnatal development of ilfs and tertiary lymphoid tissue in the si lamina propria , which can substitute for peyer 's patches as inductive sites for intestinal iga ( 38 ) . intestinal iga coating identifies inflammatory commensals that drive intestinal disease like inflammatory bowel disease ( 33,39 ) . the siga within mucus establishes distance with commensals and forms a barrier between invading and commensal microorganisms . intestinal dcs support iga isotype class - switching and differentiation into iga - secreting plasma cells , either together with the assistance of th cells or in a t cell - independent manner by expressing b cell - activating factors ( baffs ) and a proliferation - inducing ligand ( april ) ( fig . 3 ) . intestinal pdcs , in particular , have been shown to induce iga production by expressing these factors ( 40 ) . when commensal bacteria are recognized through tlrs , tip dcs release large amounts of no which enhances iga class - switch dna recombination ( csr ) in b cells by inducing dc expression of baff and april ( 13 ) . further , ra can be converted by raldh2 from dietary vitamin a in dcs , and dcs expressing raldh2 can also induce iga csr ( 41 ) . lamina propria cd103cd11b dcs , tip dcs , and tlr5 dcs express raldh2 and produce ra , which in turn can be used for iga production together with tgf- ( 13,36,42 ) . langerin - expressing dcs in the mlns that emerge following trans - cutaneous vaccination can also induce ra - dependent antigen - specific iga production in the si ( 43 ) . moreover , ra confers gut homing signature such as 47 integrin and ccr9 on lymphocytes ( 42,44 ) . therefore , ra is essential to maintaining the intestinal immune environment ( 45,46 ) . in normal lamina propria , large numbers of eosinophils are present , accounting for approximately 5% of all lamina propria leukocytes ( 47 ) . recently , eosinophils have been found to promote the generation and maintenance of iga - producing plasma cells by inducing b cell activating factors ( 48 ) and supporting the function of cd103 dcs ( 49 ) . in this review , we focused on the integral role of intestinal dcs in shaping the unique intestinal immunity . the advent of advanced experimental techniques for surveying mucosal tissues and analyzing metagenomic data of commensals , along with the wide availability of germ - free mice has facilitated a growing understanding of this unique mucosal immune environment . for example , clostridium strains provide a rich environment of tgf- and induce foxp3 treg in the colon ( 50,51 ) , and sfb induce the generation of th17 cell by il-6 production from dcs ( 32 ) . some pathogens ( e.g. , listeria spp . ) thus , microbial signals may induce polarizing cytokine secretion from dcs , other innate cells or stromal cells . assembling combined information