17-7222-82

antibody from Invitrogen Antibodies

Targeting: IL22 IL-21, IL-22, IL-D110, IL-TIF, ILTIF, MGC79382, MGC79384, TIFa, TIFIL-23, zcyto18

Provider product page for 17-7222-82

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Antibody data

Antibody Data
Antigen structure
References [42]
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Validations
Flow cytometry [1]
Other assay [17]

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Product number: 17-7222-82 - Provider product page
Provider: Invitrogen Antibodies
Product name: IL-22 Monoclonal Antibody (IL22JOP), APC, eBioscience™
Antibody type: Monoclonal
Antigen: Other
Description: Description: The monoclonal antibody IL22JOP reacts with and inhibits the bioactivity of human and mouse IL-22. IL-22 is a 20 kDa member of the IL-10 cytokine family that is secreted primarily by Th17 cells, NK cells, and other T cells. Compared to IL-6 or TGF beta, IL-23 can induce greater levels of IL-22 in in vitro-differentiated Th17 cells. This observation suggests that IL-22 may be secreted by more fully differentiated Th17 cells in vivo. Recently, it was demonstrated that IL-22 could protect hosts from bacterial infection of the lungs and gut. Moreover, it has been reported that anti-CD3/CD28-induced production of IL-22 by PBMCs was elevated significantly in asthma patients compared to control patients. Flow cytometric analysis also showed that the frequencies of IL-17+IL-22+ CD4 T cells were increased in PBMCs from patients with ankylosing spondylitis and rheumatoid arthritis.
Antibody clone number: IL22JOP
Concentration: 0.2 mg/mL

IL22 protein structure - 17-7222-82 shown in red.

Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 4 Gene profiling reveals tissue-specific transcriptomic signature of gammadeltaT17 cells. a Left panel, principal component analysis (PCA) plot of the RNA-seq of Tfam-sufficient splenic (Sp), small intestinal (SI), and large intestinal (LI) gammadeltaT17 cells from 3-week-old ( n = 3 for each group) mice. gammadeltaT17 cells of each sample were sorted from an individual mouse. Right panel, Euclidean distance comparison of the transcriptome of each splenic gammadeltaT17 cell sample and the mean intestine centroid vs. the mean small intestine centroid to each large intestinal gammadeltaT17 cell sample ( n = 3 for each group) (*** P = 0.0002). b Heatmap of tissue-specific genes (TSGs) identified by the RNA-seq in Sp, SI, and LI gammadeltaT17 cells. Genes were ranked in a descending order based on the fold changes of expression (Sp/[SI and LI average mean]; [SI and LI average mean]/Sp). c RNA-seq FPKM values of Ahr direct target genes of Sp, SI, and LI gammadeltaT17 cells (mean +- SD) ( n = 3 for each group) (Sp vs. SI: Ahr , *** P = 0.0005, Ahrr , ** P = 0.0037, Asb2 , *** P = 0.0004, Cd93 , **** P < 0.0001, Cd160 , *** P = 0.0002, Gem , ** P = 0.0096, Hic1 , *** P = 0.0002, Il17a , **** P < 0.0001, Il22 , * P = 0.0180, Kit , *** P = 0.0004, Nuerl3 , **** P < 0.0001, Osgin1 , *** P = 0.0002, Vps37b , **** P < 0.0001; Sp vs. LI: Ahr , * P = 0.0460, Ahrr , P = 0.0506, Asb2 , ** P = 0.0076, Cd93 , **** P < 0.0001, Cd160 , *** P = 0.0001, Gem , * P = 0.0108, Hic1 , *** P = 0.00

Supportive validation

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Experimental details: Figure 1 CXCL4 increases the percentage of IL-17 producing cells in CD3/CD28-stimulated human CD4 + T cells. CD4 + T cells were isolated from healthy donors and cultured with CD3/CD28 coated Dynabeads and CXCL4 for five days. (A, B) The effect of CXCL4 on IL-17 production by CD4 + T cells was assessed by (A) flow cytometric intracellular cytokine staining and (B) enzyme-linked immunosorbent assay. (C) The percentage of of IFN-gamma-, IL-4- and IL-22-producing CD4 + T cells were measured by flow cytometry. (D, E) The amount of IL-17 producing cells co-expressing IFN-gamma (D) or IL-22 (E) were measured by flow cytometry. Cells were gated on live, single cells. Means (bars) and values from each donor are shown. Data are pooled from two to four independent experiments, except for panel B from 14 independent experiments, with one to four donor samples per experiment. Each dot on the bar graphs represent a single donor and paired t -test was used for statistical analysis. * p

Supportive validation

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Experimental details: Figure 2 CXCL4 induces IL-17 producing cells differentiated from naive human CD4 + T cells. Naive CD4 + T cells were purified by fluorescence-activated cell sorting and cultured with CD3/CD28 coated Dynabeads and CXCL4 for seven days. (A, B) The effect of CXCL4 on IL-17 production by CD4 + T cells was assessed by (A) flow cytometric intracellular cytokine staining and (B) enzyme-linked immunosorbent assay. (C) The levels of IFN-gamma-, IL-4-, IL-22-, and IL-17/IFN-gamma-producing CD4 + T cells were measured by flow cytometry. (D) The amount of IL-17 producing cells co-expressing or IL-22 was measured by flow cytometry. Cells were gated on live, single cells. Means (bars) and values from each donor are shown. Data are pooled from four to 10 independent experiments, with one to two donor samples per experiment. Each dot on the bar graphs represents a single donor and paired t -test was used for statistical analysis. * p

Supportive validation

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Experimental details: Figure 4 CXCL4-differentiated monocyte-derived dendritic cells enhance pro-inflammatory cytokine production and proliferation by CD4 + T cells. Monocytes from healthy donors were isolated and differentiated into dendritic cells in the absence or presence of CXCL4 (moDCs or CXCL4-moDCs). moDCs were then co-cultured with autologous CD4 + T cells in the presence of superantigen from Staphylococcal Enterotoxin B (SEB) for three days and restimulated with PMA and ionomycin. (A-C) Comparison of co-culture with moDC or CXCL4-moDC on IL-17 or IFN-gamma production by CD4 + T cells was assessed by (A, C) intracellular cytokine staining and (B) enzyme-linked immunosorbent assay are shown. (D) Intracellular cytokine staining was performed for the measurement of IL-4 + , IL-10 + , IL-22 + , and IL-17 + IFN-gamma + cells gated on live CD4 + T cells. (E) The amount of IL-17 producing cells co-expressing IL-22 as measured by flow cytometry. (F) CD4 + T cells were labeled with CellTrace Violet prior co-culture and proliferation was analyzed as division index. Cells were gated on live, single, CD4 + T cells. Means (bars) and values from each donor are shown. Data are pooled from two to three independent experiments, with two to three donor samples per experiment. Each dot on the bar graphs represent a single donor and paired t -test was used for statistical analysis. * p

Supportive validation

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Experimental details: Figure 9 LCN2 reduces intestinal adaptation by inhibiting IL22 expression after 75% SBR on POD 7 . ( A ) IL22 protein expression in the serum was measured by ELISA (n = 7 mice per group). ( B ) Transcriptional levels of the Il22 gene in the intestine were evaluated by quantitative PCR (n = 6 per group). ( C ) CD4 + IL22 + LPLs were quantified with flow cytometry analysis (n = 5 per group). ( D ) Representative IL22 protein expression in supernatant from Th22 cells in vitro with and without LCN2 stimulation as measured by ELISA (n = 3 per group/each experiment, each experiment was repeated 3 times). ( E-H ) Representative flow cytometry dot plots of the LPL population from small intestinal tissue. Single-cell suspensions prepared from the lamina propria were stained with CD4 and IL22 antibodies. Gate 1 identified lymphocytes based on FSC-A/SSC-A properties. The numbers within the quadrants represent the percentage of CD4 + IL22 - , CD4 + IL22 + , CD4 - IL22 - , and CD4 - IL22 + cells within the lymphocyte gate. Data are representative of analyses of 5 mice per group. Forward scatter area (FSC-A)/side scatter area (SSC-A). * P < .05, ** P < .01, and *** P < .001.

Supportive validation

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Experimental details: Figure 1 Imiquimod increases IL-17 and IL-22 in both gammadelta and alphabeta T cells in skin. Skin and ear of wild type C57BL/6 mice were treated by topical application of imiquimod cream (Fougera, n =4) or control cream (Vaseline, n =3) for 6 consecutive days. ( a ) Weight loss of imiquimod and control cream treated mice monitored daily. ( b ) Photographs of imiquimod and control cream treated skin and ear; photos were taken at day 6. H&E stained ear and back skin sections of imiquimod treated and control mice. Scale bar, 200 mum. ( c ) Thickness of skin measured by Digimatic Caliper at day 6 in control and imiquimod treated mice. Data showed represents average of at least two measurements. ( d ) Ear thickness of imiquimod and control cream treated mice monitored daily. Ear thickness was measured using Digimatic Caliper. ( e ) Quantitative PCR analysis of Th17 associated cytokines and Foxp3 in skin after 6 days of imiquimod and control cream treatment. ( f ) Representative flow cytometric analysis of TCRgammadelta + Vgamma4 + IL-17 + (upper raw) and TCRgammadelta + Vgamma4 + IL-22 + cells (lower row) in the skin of control ( n =3) and imiquimod treated mice ( n =4). ( g ) Representative flow cytometric analysis of single-positive TCRbeta + IL-17 + (upper raw) or TCRbeta + IL-22 + (lower raw) cells in the skin of control ( n =3) and imiquimod treated mice ( n =4). Data representative of more than three experiments, results are shown as mean+-s.e.m., significance determined b

Supportive validation

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Experimental details: Figure 2 Antibiotics in adult mice ameliorate psoriasis by reduction of IL-17 and IL-22 in T cells. Young adult mice (4-weeks-old) were exposed to antibiotics in drinking water (adultATB) for four weeks, and last six consecutive days followed by imiquimod treatment. ( a ) Representative photographs of back skin of control and adultATB mice followed by imiquimod treatment. Photos were taken at day 6. ( b ) H&E stained skin sections of control and adultATB mice after imiquimod treatment. Scale bar, 200 mum. ( c ) Thickness of skin measured by digimatic caliper at day 6 in control and imiquimod treated mice. Data showed represents average of at least two measurements. Increased skin infiltration in control compared adultATB mice based on staining of skin CD45 + cells. ( d ) Flow cytometric analysis of single-positive CD3 + TCRgammadelta low+ IL-17 + cells or CD3 + TCRgammadelta - IL-17 + cells in control ( n =6-7) and adultATB ( n =6-7) mice after imiquimod treatment. ( e ) Flow cytometric analysis of single-positive CD3 + TCRgammadelta low+ IL-22 + cells or CD3 + TCRgammadelta - IL-22 + cells in control ( n =6) and adultATB ( n =6) mice after imiquimod treatment. ( f ) Frequency of skin CD3 + TCRbeta + Foxp3 + cells in the skin of control ( n =5) and adultATB ( n =7) mice after imiquimod treatment. ( g ) Diversity of the microbiota (Observed OTUs, Shannon Index) in adultATB and control mice. Primary samples were collected per cage (Pooled samples from 3 independent experiments)

Supportive validation

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Experimental details: Figure 3 Neonatal antibiotic treatment of mice increases severity of psoriasis. Breeding pairs were given antibiotics vancomycin+polymyxin B in drinking water immediately after pups delivery for 3 weeks of rearing (neoATB). After weaning, mice were housed or cohoused (mice without antibiotics treatment together with mice treated with antibiotics) in normal specific pathogen-free conditions for next 8 weeks. The mice were then treated with imiquimod cream for 4 consecutive days. ( a ) Representative photographs of back skin in controls (mice without antibiotic treatment); neonatally antibiotics treated mice (neoATB) or cohoused mice (control-neoATB resp. NeoATB-control) after imiquimod treatment. Photos were taken at day 5. ( b ) H&E stained skin sections of control, neoATB and cohoused mice after imiquimod treatment. Scale bar, 200 mum. ( c ) Weight loss of control, neoATB and cohoused mice during imiquimod treatment monitored daily. ( d ) Skin thickness of control, neoATB and cohoused mice measured at day 5. Skin thickness was measured by digimatic caliper by at least two investigators and data showed represents average of at least two measurements. ( e ) Flow cytometric analysis of single-positive TCRgammadelta + Vgamma4 + IL-17 + cells or CD3 + TCRbeta + IL-17 + cells in control ( n =8), neoATB ( n =7) and cohoused mice ( n =5) after imiquimod treatment. ( f ) Flow cytometric analysis of single-positive TCRgammadelta + Vgamma4 + IL-22 + cells or CD3 + TCRbeta + IL-22 + cel

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 7 ATF3 promotes IL-22-induced STAT3 phosphorylation by suppressing phosphatases. (A) Freshly isolated ileum crypts, or (B) ileum organoids at day 6 of culture, were stimulated with IL-22, followed by fixation and intracellular staining of phospho-STAT3, and analyzed by flow cytometry. Western blot analysis of (C) IL-22-stimulated CMT93 cells, or (D) IL-22-stimuated colon fragments isolated from the indicated mice, for the expression of the indicated proteins. (E) Quantitative real-time PCR analysis of IL-22R1 and IL-10R2 mRNA levels in freshly isolated ileum crypts from mice. (F) Flow cytometry analysis of IL-22R1 in freshly isolated ileum crypt cells gated on the CD45 - EpCAM + population. (G,H) Western blot analysis of unstimulated or IL-22-stimulated CMT93 cells for the indicated proteins. ATF3 -/- CMT93 cells with SHP2 knockdown (ATF3 -/- SHP2 KD ) were indicated. Images were representative of four independent experiments (G-H) . Results were from two independent experiments (A-F) . ""n"" refers to the number of mice analyzed (A,B,E,F) . Statistical analysis was done by multiple comparison in Two-way ANOVA test using Prism software. * P < 0.05, ** P < 0.005, *** P < 0.0005.

Supportive validation

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Experimental details: Figure 8 ATF3 regulates IL-6-pSTAT3 signaling in intestinal Th17 cells. Flow cytometry analysis of phospho-STAT3 in (A) IL-6 or IL-22 stimulated freshly isolated ileum crypts or IL-6-stimulated peripheral blood mononuclear cell (PBMC) from wild-type mice, or in (B) IL-6-stimulated PBMC from wild-type and ATF3-deficient mice. (C) Flow cytometry analysis of intracellular IL-17A and IL-22 expression in naive lamina propria T cells from the indicated mice. Cells were treated with PMA, ionomycin and IL-23 in the presence of BFA for 4 h before analysis and gated on live CD45 + EpCAM - Lin - CD3 + population as shown. (D) Quantitative real-time PCR analysis of IL-17A and IL-22 mRNA levels in freshly isolated lamina propria (LPL) cells, mesenteric lymph nodes (mLN), or splenocytes. (E) Model of ATF3-mediated mucosal immunity via cross-regulation between IL-22-pSTAT3 signaling in epithelium (associated with AMP production and epithelial fucosylation) and IL-6-pSTAT3 signaling in Th17 cells (associated with signature IL-17A and IL-22 production). ""n"" refers to the number of mice analyzed. Statistical analysis was done by multiple comparison in Two-way ANOVA test using Prism software. * P < 0.05, ** P < 0.005, *** P < 0.0005.

Supportive validation

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Experimental details: 5 FIGURE Flow cytometry revealed central memory T cell, Th1, Th17, Th22 and Treg proportions increased in PBMCs derived from CP/CPPS patients than healthy controls. PBMCs were incubated with various fluorescein-labelled antigens for surface staining. PerCP/Cyanine5.5-conjugated CD3 and FITC-conjugated CD4 were used for the central memory T cell, Th1, Th17 and Th22 cell staining, and PE-conjugated CD25 and FITC-conjugated CD4 were incubated for staining Treg cells. After fixing and permeabilizing with cell fixation/permeabilization kit, (A) for samples staining central memory T cells were incubated with PE-conjugated CD45RA and APC-conjugated CD62L; (C) for samples staining, Th1 cells were incubated with PE-conjugated IFN-gamma; (E) for samples staining, Treg cells were incubated with eFluor 660-conjugated FoxP3; (G) for samples staining, Th17 cells were incubated with PE-conjugated IL-17A; and (I) for samples staining, Th22 cells were incubated with PE-conjugated IL-17A and APC-conjugated IL-22. The quantification data were presented in B, D, F, H and J. * P < 0.05; PBMC, peripheral blood mononuclear cell