IMMUNOLOGICAL TOLERANCE TO A HAPTEN

Treatment of mice with a nonimmunogenic preparation of free reactive hapten, trinitrobenzene sulfonic acid (TNBS), leads to the induction of a state of tolerance to the hapten, 2,4,6-trinitrophenyl (TNP). This is determined by the lack of response to the haptenic moiety in an immunogenic hapten-carrier conjugate (TNP-SRBC) as assayed both by serum antibody titrations and the hemolytic plaque assay. The tolerance produced is specific for the hapten, since the anticarrier responses are essentially unaltered compared with the control values. The unresponsiveness induced by TNBS treatment is a dose-dependent phenomenon, becoming less complete at lower doses of TNBS. The tolerance is of a definite length, both in its induction phase and in the duration of the established unresponsive state. Tolerance can be maintained and extended, and may also be reentered once escape has been initiated.

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A colon epithelial protein(s) induces oral tolerance in a dose dependent manner in the trinitrobenzene sulfonic acid (TNBS) model of colitis in rats

Gastroenterology ◽

10.1016/s0016-5085(01)81385-8 ◽

2001 ◽

Vol 120 (5) ◽

pp. A279-A279

Author(s):

A DASGUPTA ◽

J GIRALDO ◽

P AMENTA ◽

K DAS

Keyword(s):

Sulfonic Acid ◽

Oral Tolerance ◽

Protein S ◽

Trinitrobenzene Sulfonic Acid ◽

Dependent Manner ◽

Dose Dependent

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Dose‐dependent effects of kefir on colitis induced by trinitrobenzene sulfonic acid in rats

Food Science & Nutrition ◽

10.1002/fsn3.1174 ◽

2019 ◽

Vol 7 (9) ◽

pp. 3110-3118

Author(s):

Nurhayat Ozkan Sevencan ◽

Mehmet Isler ◽

Fatma Nilgun Kapucuoglu ◽

Altug Senol ◽

Burcak Kayhan ◽

...

Keyword(s):

Sulfonic Acid ◽

Trinitrobenzene Sulfonic Acid ◽

Dose Dependent

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A colon epithelial protein(s) induces oral tolerance in a dose dependent manner in the trinitrobenzene sulfonic acid (TNBS) model of colitis in rats

Gastroenterology ◽

10.1016/s0016-5085(08)81385-6 ◽

2001 ◽

Vol 120 (5) ◽

pp. A279

Author(s):

Arunansu Dasgupta ◽

Jorge Giraldo ◽

peter S. Amenta ◽

Kiron M. Das

Keyword(s):

Sulfonic Acid ◽

Oral Tolerance ◽

Protein S ◽

Trinitrobenzene Sulfonic Acid ◽

Dependent Manner ◽

Dose Dependent

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Inhibition of p38 Mitogen-Activated Protein Kinase Impairs Mayaro Virus Replication in Human Dermal Fibroblasts and HeLa Cells

Viruses ◽

10.3390/v13061156 ◽

2021 ◽

Vol 13 (6) ◽

pp. 1156

Author(s):

Madelaine Sugasti-Salazar ◽

Yessica Y. Llamas-González ◽

Dalkiria Campos ◽

José González-Santamaría

Keyword(s):

Protein Expression ◽

Hela Cells ◽

Plaque Assay ◽

Dermal Fibroblasts ◽

Dependent Manner ◽

Human Dermal Fibroblasts ◽

Mitogen Activated Protein ◽

Mayaro Virus ◽

The Impact ◽

Dose Dependent

Mayaro virus (MAYV) hijacks the host’s cell machinery to effectively replicate. The mitogen-activated protein kinases (MAPKs) p38, JNK, and ERK1/2 have emerged as crucial cellular factors implicated in different stages of the viral cycle. However, whether MAYV uses these MAPKs to competently replicate has not yet been determined. The aim of this study was to evaluate the impact of MAPK inhibition on MAYV replication using primary human dermal fibroblasts (HDFs) and HeLa cells. Viral yields in supernatants from MAYV-infected cells treated or untreated with inhibitors SB203580, SP600125, U0126, or Losmapimod were quantified using plaque assay. Additionally, viral protein expression was analyzed using immunoblot and immunofluorescence. Knockdown of p38⍺/p38β isoforms was performed in HDFs using the PROTACs molecule NR-7h. Our data demonstrated that HDFs are highly susceptible to MAYV infection. SB203580, a p38 inhibitor, reduced MAYV replication in a dose-dependent manner in both HDFs and HeLa cells. Additionally, SB203580 significantly decreased viral E1 protein expression. Similarly, knockdown or inhibition of p38⍺/p38β isoforms with NR-7h or Losmapimod, respectively, affected MAYV replication in a dose-dependent manner. Collectively, these findings suggest that p38 could play an important role in MAYV replication and could serve as a therapeutic target to control MAYV infection.

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