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1 s (ie, interferon gamma, interleukin 17, and interleukin 22).
2 ytokines (interleukin-4, interleukin-17, and interleukin-22).
3 -type lectins Reg3gamma and Reg3beta, and of interleukin 22.
4 ncluding interleukin 10, interleukin 13, and interleukin 22.
5 phage-epithelial cell cross-talk mediated by interleukin-22.
6 ing higher levels of the reparative cytokine interleukin-22.
7 vation of TLR5 on DCs leads to production of interleukin-22.
8 ing the interleukin-23/T helper 17 cytokine, interleukin-22.
9 lete loss of flagellin-induced production of interleukin-22.
10 r necrosis factor-alpha, interleukin-17, and interleukin-22.
11 was an inverse association between levels of interleukin 22 and serum levels of tryptophan.
12                     The relationship between interleukin-22 and clinical characteristics of patients
13        This induction required the cytokines interleukin-22 and lymphotoxin in a commensal bacteria-d
14 actions of CD4+ T cells, higher fractions of interleukin 22, and a tendency to higher fractions of in
15              Human CD4+ T cells that produce interleukin 22 are an essential component of skin defens
16                       Serum concentration of interleukin 22 associated with disease activity in patie
17  836 with ulcerative colitis had non-missing interleukin-22 baseline samples, of which 33% and 25%, r
18 in those with high interleukin-22 versus low interleukin-22 (below lower limit of quantification).
19 rs exhibited low levels of tumor-suppressive interleukin-22 binding protein (IL-22BP) compared to nor
20 rom patients with IBD produce high levels of interleukin-22 binding protein (IL-22BP), the endogenous
21 h increased expression of interleukin-17 and interleukin-22 by day 5 after injury.
22  Immunity, Kryczek et al. (2014) reveal that interleukin-22 can also promote "stemness" in human colo
23 th moderate/severe disease activity had high interleukin-22 concentrations (above lower limit of quan
24        We sought to determine whether plasma interleukin-22 concentrations are associated with diseas
25             The strongest predictors of high interleukin-22 concentrations identified by a machine-le
26                             In summary, high interleukin-22 concentrations tended to be associated wi
27                                              Interleukin-22 concentrations were measured using an R&D
28        Human ILC3s that produce the cytokine interleukin-22 convert into ILC1-like cells that produce
29 tective measures against such events include interleukin-22-driven systemic elimination of pathobiont
30 ons were measured using an R&D Systems human interleukin-22 enzyme-linked immunosorbent assay.
31 n in hematopoietic cells and is dependent on interleukin 22 expression.
32                                              Interleukin 22 (IL-22) has a non-redundant role in immun
33 e T cells homed to skin, where they produced interleukin 22 (IL-22) in response to CD1a on Langerhans
34                    Previously, we found that interleukin 22 (IL-22) inhibits intracellular growth of
35                                              Interleukin 22 (IL-22) is a member of the IL-10 cytokine
36                                              Interleukin 22 (IL-22) is an IL-10-related cytokine prod
37                                              Interleukin 22 (IL-22) is emerging as a key cytokine for
38                      Studies have shown that interleukin 22 (IL-22) is expressed at barrier surfaces
39 ntestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production.
40                                              Interleukin 22 (IL-22) promotes intestinal barrier integ
41 ), since mice deficient in IFN-gamma but not interleukin 22 (IL-22) signaling pathways rescued chlamy
42                                              Interleukin 22 (IL-22) signals via both IL-22 receptor a
43 ulosis for 24 hours yielded higher IL-10 and interleukin 22 (IL-22) transcript levels for tuberculosi
44                                              Interleukin 22 (IL-22), a cytokine of the IL-10 superfam
45             Here we investigated the role of interleukin 22 (IL-22), an IL-10 family member whose rec
46 nterleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 22 (IL-22), and tumor necrosis factor alpha
47                                              Interleukin 22 (IL-22), which is produced by cells of th
48 ntestinal mucosa from infection by secreting interleukin 22 (IL-22).
49                   The mechanism of action of interleukin- 22 (IL-22) in inflammatory arthritis remain
50                                              Interleukin-22 (IL-22) acts on epithelial cells to promo
51                                              Interleukin-22 (IL-22) and IL-17A are both effector cyto
52 heir association with the signaling proteins interleukin-22 (IL-22) and transforming growth factor be
53 e (Bcl-xl) levels and their association with interleukin-22 (IL-22) and transforming growth factor be
54      We detail such a mechanism, centered on interleukin-22 (IL-22) and triggered by the depletion of
55 ells (ILC3s) support gut homeostasis through interleukin-22 (IL-22) but can convert into interferon-g
56  ILC3s resulted in deficiency of intrathymic interleukin-22 (IL-22) compared with transplant recipien
57 , CD4(+) LTi cells were a dominant source of interleukin-22 (IL-22) early during infection.
58                                              Interleukin-22 (IL-22) exerts both protective and pathog
59 athogen, Citrobacter rodentium, we show that interleukin-22 (IL-22) has a crucial role in the early p
60                                              Interleukin-22 (IL-22) has important functions in host d
61  community-acquired pneumonia worldwide, and interleukin-22 (IL-22) helps contain pneumococcal burden
62                               Reduced innate interleukin-22 (IL-22) in Ahr-deficient mice allowed exp
63 y, a subset of T helper (Th) cells producing interleukin-22 (IL-22) in breast and lung tumors is link
64                              The function of interleukin-22 (IL-22) in intestinal barrier homeostasis
65                             Here we detected interleukin-22 (IL-22) in patient colorectal cancer tiss
66 thway in which innate lymphoid cells produce interleukin-22 (IL-22) in response to loss of double pos
67          Here, we report a critical role for interleukin-22 (IL-22) in systemic protection against ba
68                                              Interleukin-22 (IL-22) is a critical immune defence cyto
69                                 The cytokine interleukin-22 (IL-22) is a critical regulator of epithe
70                                              Interleukin-22 (IL-22) is a recently described IL-10 fam
71                                              Interleukin-22 (IL-22) is a T helper 17 (Th17) T cell-as
72                                              Interleukin-22 (IL-22) is central to host protection aga
73                                              Interleukin-22 (IL-22) is considered indispensable for h
74                                              Interleukin-22 (IL-22) is highly induced in response to
75                                 The cytokine interleukin-22 (IL-22) is primarily expressed by T helpe
76                                              Interleukin-22 (IL-22) is released by immune cells and m
77 fection, and mice with and without exogenous interleukin-22 (IL-22) or anti-IL-22 antibodies.
78                                              Interleukin-22 (IL-22) plays a critical role in mucosal
79                                              Interleukin-22 (IL-22) plays an important role in host i
80                                 For example, interleukin-22 (IL-22) production by group 3 innate lymp
81                             Acetate enhances interleukin-22 (IL-22) production by ILC3s, which then s
82  reported that intermittent fasting promoted interleukin-22 (IL-22) production by type 3 innate lymph
83  these profiles, with a nearly total loss of interleukin-22 (IL-22) production in the tonsil and colo
84 g HFD with inulin restored microbiota loads, interleukin-22 (IL-22) production, enterocyte proliferat
85 their in situ proliferation and ILC3-derived interleukin-22 (IL-22) production.
86 arly colonization resistance was mediated by interleukin-22 (IL-22) regulation of the microbiota.
87 trained" ILC3s proliferate, display enhanced interleukin-22 (IL-22) responses, and have a superior ca
88 ain subset of dendritic cells and increasing interleukin-22 (IL-22) secretion.
89 ously identified human ILC3 distinguished by interleukin-22 (IL-22) secretion.
90       We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelia
91                                              Interleukin-22 (IL-22), a recently identified member of
92 rotective role in liver disease by releasing interleukin-22 (IL-22), a recently identified T cell-der
93 t induction of gamma interferon (IFN-gamma), interleukin-22 (IL-22), and IL-17 expression (genes Ifn-
94 forming growth factor beta, forkhead box P3, interleukin-22 (IL-22), and IL-17 mRNA but caused minima
95 genes encoding gamma interferon (IFN-gamma), interleukin-22 (IL-22), and IL-17 were detected by quant
96                   This occurs independent of interleukin-22 (IL-22), and we identify that ILC3s are a
97 gulation of proinflammatory genes, including interleukin-22 (IL-22), in the epithelial cells of Pgr(d
98               Here we show that the cytokine interleukin-22 (IL-22), produced by group 3 innate lymph
99  express aryl hydrocarbon receptor (AHR) and interleukin-22 (IL-22), supporting a role in mucosal imm
100 irmed that NKp44(+) ILC3 produced protective interleukin-22 (IL-22), whereas ILC1s produced proinflam
101 irmed that NKp44(+) ILC3 produced protective interleukin-22 (IL-22), whereas ILC1s produced proinflam
102                                              Interleukin-22 (IL-22), which acts as either a proinflam
103 ic cells elicited production of the cytokine interleukin-22 (IL-22), which induced a protective gene
104 how here that attenuated ileitis observed in interleukin-22 (IL-22)-deficient mice was associated wit
105  activation of the aryl hydrocarbon receptor-interleukin-22 (IL-22)-IL-10 host pathway and the produc
106 an secondary lymphoid tissues (SLTs) contain interleukin-22 (IL-22)-producing cells with an immature
107                           Here, we show that interleukin-22 (IL-22)-producing innate lymphoid cells (
108 alphabeta(+) T cells and their production of interleukin-22 (IL-22).
109 heir homeostasis and driving them to produce interleukin-22 (IL-22).
110 ut immunity presumably through production of interleukin-22 (IL-22).
111                Our studies revealed that the interleukin-22 (IL-22)/IL-17-producing ILCS was not alte
112 pression of interferon gamma (IFN-gamma) and interleukin-22 (IL-22); these cytokine loci are closely
113       Similar differences were observed with interleukin 22 (IL22) mRNA showing early downregulation
114 ti-CD40 murine colitis models in response to interleukin-22 immunoglobulin Fc (IL22Fc) fusion protein
115                        We measured levels of interleukin 22 in serum from 28 patients by enzyme-linke
116 ; and interleukin 6, interleukin 10, IL-17A, interleukin 22, interleukin 23, interferon gamma, kynure
117  and c-MAF, driving heightened production of interleukin-22, interleukin-10, and granzyme B.
118 y different colonic cytokine profiles (e.g., interleukin-22, interleukin-17, interferon-y, or granulo
119                                              Interleukin-22 is produced by certain T helper cells sub
120 edly downregulated in DM, but not sIBM, were interleukin 22, Kallmann syndrome 1 (KAL-1), an adhesion
121 tional markers (interferon-y, interleukin 4, interleukin 22, latency associated peptide-transforming
122              Interestingly, higher levels of interleukin 22, monocyte chemoattractant protein 1, TNF-
123 red on several distinct cell axes, including interleukin-22 produced by innate lymphoid cells, BMP4 b
124 silosis induced much less interleukin 17 and interleukin 22 production as compared to C. albicans.
125 wever, RORa was sufficient to support robust interleukin-22 production among the lymphoid tissue indu
126 ated this program through the suppression of interleukin-22 production by type 3 innate lymphoid cell
127  helper 17 (T(H)17) phenotype and stimulated interleukin-22 production, which reduced intestinal fat
128                  We show that the epithelial interleukin-22 receptor IL-22RA1 protects against lethal
129 show that a network including the epithelial interleukin-22 receptor protects against infection with
130 culum (ER) stress, using animals lacking the interleukin-22-receptor (IL-22RA1), primary human and mu
131 tance, altered bile acid metabolism, reduced interleukin-22 secretion and infertility.
132 onstrate that mice lacking IL-17RA, Act1, or interleukin 22 showed no evidence for altered VVC suscep
133 activation, likely through intestinal IL-22 (interleukin-22) signaling.
134 , which was in turn linked to perturbed host interleukin-22 signalling and epithelial cell apoptosis
135 mately 200-fold expansion of interleukin 17+/interleukin 22+ T effectors with profound Th1 suppressio
136 e/severe disease activity in those with high interleukin-22 versus low interleukin-22 (below lower li
137 nra arm was decreased, and the production of interleukin 22 was increased.
138 in mice and production of interleukin-17 and interleukin-22 were found to be critical inducers of lun
139 nt and survival, and produced high levels of interleukin-22, which prevented liver damage.
140 hnsen et al. (2014) report that the cytokine interleukin-22, which usually plays a protective role, p
141 he cytokines measured (with the exception of interleukin 22) with hemoglobin A1c levels.

 
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