Rabbit ileal lamina propria mononuclear cells suppress the primary in vitro antibody response of spleen cells to KLH

Using anin vitroautologous human system, the immunomodulatory function of colonic intraepithelial lymphocytes (IEL) on cytokine production by lamina propria mononuclear cells (LPMNC) has been investigated. In contrast to LPMNC, colonic IEL produced only low amounts of IL-10, interferon-γ and interleukin-2. However, co-culture experiments (IEL + LPMNC) have shown that IEL can enhance the PHA-induced synthesis of IL-2 and interferon-γ, but not IL-10 by LPMNC. Using a transwell filter culture system apparatus, this effect was shown not to require a cell-to-cell interaction. Thus, IELin vitromay modulate the cytokine synthesis of LPMNC, through the production of soluble factors. This may prove highly relevant in thein vivoimmune activation of the gastrointestinal mucosa.

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In vitro immunomodulation of RH IL-10 on TNF-α secretion by lamina propria mononuclear cells in Crohn's disease

Gastroenterology ◽

10.1016/s0016-5085(98)84390-4 ◽

1998 ◽

Vol 114 ◽

pp. A1079

Author(s):

A. Schmit ◽

M. Carol ◽

A. Van Gossum ◽

M. Goldman ◽

F. Mascart-Lemone

Keyword(s):

Crohn’S Disease ◽

Crohn's Disease ◽

Lamina Propria ◽

Mononuclear Cells ◽

Lamina Propria Mononuclear Cells ◽

Tnf Α

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Spontaneous secretion of interferon γ and interleukin 4 by human intraepithelial and lamina propria gut lymphocytes

Gut ◽

10.1136/gut.42.5.643 ◽

1998 ◽

Vol 42 (5) ◽

pp. 643-649 ◽

Cited By ~ 64

Author(s):

M Carol ◽

A Lambrechts ◽

A Van Gossum ◽

M Libin ◽

M Goldman ◽

...

Keyword(s):

Lamina Propria ◽

Intestinal Mucosa ◽

Mononuclear Cells ◽

Critical Role ◽

Gastrointestinal Diseases ◽

Interferon Γ ◽

Interleukin 4 ◽

Peripheral Blood Mononuclear ◽

Ifn Γ

Background—Cytokines secreted by intestinal T lymphocytes probably play a critical role in regulation of the gut associated immune responses.Aims—To quantify interferon γ (IFN-γ) and interleukin 4 (IL-4) secreting cells (SC) among human intraepithelial (IEL) and lamina propria (LPL) lymphocytes from the duodenum and right colon in non-pathological situations and in the absence of in vitro stimulation.Patients—Duodenal and right colonic biopsy specimens were obtained from patients with no inflammation of the intestinal mucosa.Methods—Intraepithelial and lamina propria cell suspensions were assayed for numbers of cells spontaneously secreting IFN-γ and IL-4 by a two site reverse enzyme linked immunospot technique (ELISPOT).Results—The relatively high proportion of duodenal lymphocytes spontaneously secreting IFN-γ (IEL 3.6%; LPL 1.9%) and IL-4 (IEL 1.3%; LPL 0.7%) contrasted with the very low numbers of spontaneously IFN-γ SC and the absence of spontaneously IL-4 SC among peripheral blood mononuclear cells. In the basal state, both IFN-γ and IL-4 were mainly produced by CD4+ cells. Within the colon, only 0.2% of IEL and LPL secreted IFN-γ in the basal state, and 0.1% secreted IL-4.Conclusions—Compared with peripheral lymphocytes substantial proportions of intestinal epithelial and lamina propria lymphocytes spontaneously secrete IFN-γ and/or IL-4. These cytokines are probably involved in the normal homoeostasis of the human intestinal mucosa. Disturbances in their secretion could play a role in the pathogenesis of gastrointestinal diseases.

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Activation of human lamina propria mononuclear cells in inflammatory bowel disease

Advances in Mucosal Immunology ◽

10.1007/978-94-009-1848-1_209 ◽

1990 ◽

pp. 675-680 ◽

Cited By ~ 2

Author(s):

S Scheiber ◽

G S Nash ◽

S Schloemann ◽

M Bertovich ◽

J Gamero ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Lamina Propria ◽

Bowel Disease ◽

Mononuclear Cells ◽

Lamina Propria Mononuclear Cells ◽

Inflammatory Bowel

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Restoration of the in vitro antibody response of cortisone-treated spleen cells by T cells or soluble factors

Cellular Immunology ◽

10.1016/0008-8749(74)90002-1 ◽

1974 ◽

Vol 11 (1-3) ◽

pp. 11-18 ◽

Cited By ~ 14

Author(s):

Douglas C. Vann

Keyword(s):

T Cells ◽

Antibody Response ◽

Spleen Cells ◽

Soluble Factors

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Generation of FOXP3+ Inducible Regulatory T Cells by Lamina Propria Mononuclear Cells in Inflammatory Bowel Disease

Gastroenterology ◽

10.1016/s0016-5085(11)62043-x ◽

2011 ◽

Vol 140 (5) ◽

pp. S-494

Author(s):

Christopher J. Moran ◽

Scott B. Snapper

Keyword(s):

Inflammatory Bowel Disease ◽

T Cells ◽

Regulatory T Cells ◽

Lamina Propria ◽

Bowel Disease ◽

Mononuclear Cells ◽

Lamina Propria Mononuclear Cells ◽

Inflammatory Bowel

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Zinc Deficiency Activates the IL-23/Th17 Axis to Aggravate Experimental Colitis in Mice

Journal of Crohn s and Colitis ◽

10.1093/ecco-jcc/jjz193 ◽

2019 ◽

Vol 14 (6) ◽

pp. 856-866 ◽

Cited By ~ 4

Author(s):

Yasuki Higashimura ◽

Tomohisa Takagi ◽

Yuji Naito ◽

Kazuhiko Uchiyama ◽

Katsura Mizushima ◽

...

Keyword(s):

Bone Marrow ◽

Lamina Propria ◽

Zinc Deficiency ◽

Mononuclear Cells ◽

Interferon Regulatory Factor ◽

Nuclear Accumulation ◽

Regulatory Factor ◽

Colonic Inflammation ◽

Interferon Regulatory Factor 5 ◽

Lamina Propria Mononuclear Cells

Abstract Background and Aims Patients with inflammatory bowel disease [IBD], especially Crohn’s disease, often develop zinc deficiency. However, the precise mechanisms by which zinc deficiency affects IBD pathology, particularly intestinal macrophage function, remain unclear. We studied the effects of zinc deficiency on the development and progression of colitis in mice. Methods To induce colitis, mice were treated with 2,4,6-trinitrobenzene sulphonic acid. Rag1−/− mice were then given injections of naïve CD4+CD62L+ T cells. The respective degrees of mucosal injury of mice that had received a zinc chelator (TPEN; N,N,N′,N′-tetrakis [2-pyridylmethyl]ethylenediamine) and of control mice were subsequently compared. Colonic lamina propria mononuclear cells were isolated by enzymatic digestion and were examined using flow cytometry. To generate mouse bone marrow-derived macrophages [BMDMs], bone marrow cells were stimulated with mouse macrophage-colony stimulating factor. Results Zinc deficiency aggravates colonic inflammation through the activation of type 17 helper T [Th17] cells in mice. Flow cytometric analysis revealed that zinc deficiency significantly increases the proportion of pro-inflammatory [M1] macrophages in colonic lamina propria mononuclear cells obtained from inflamed colon. Interferon-γ plus lipopolysaccharide-mediated M1 skewing alters the expression of zinc transporters in BMDMs and thereby decreases the intracellular free zinc. TPEN treatment mimicking the effects of the M1 skewing up-regulates IL-23p19 expression, which is strongly related to Th17 development. Furthermore, the nuclear accumulation of interferon-regulatory factor 5 is closely involved in IL-23p19 induction in zinc-deficient macrophages. Conclusions Zinc deficiency aggravates colonic inflammation through activation of the IL-23/Th17 axis. This activation is controlled by subcellular distribution of interferon-regulatory factor 5.

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