RGD Reference Report - Thymic Stromal Lymphopoietin Is Critical for Regulation of Proinflammatory Cytokine Response and Resistance to Experimental Trypanosoma congolense Infection. - Rat Genome Database

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Thymic Stromal Lymphopoietin Is Critical for Regulation of Proinflammatory Cytokine Response and Resistance to Experimental Trypanosoma congolense Infection.

Authors: Onyilagha, Chukwunonso  Singh, Rani  Gounni, Abdelilah Soussi  Uzonna, Jude Ezeh 
Citation: Onyilagha C, etal., Front Immunol. 2017 Jul 14;8:803. doi: 10.3389/fimmu.2017.00803. eCollection 2017.
RGD ID: 38549587
Pubmed: PMID:28769924   (View Abstract at PubMed)
PMCID: PMC5509795   (View Article at PubMed Central)
DOI: DOI:10.3389/fimmu.2017.00803   (Journal Full-text)

African trypanosomiasis (sleeping sickness) poses serious threat to human and animal health in sub-Saharan Africa. Because there is currently no vaccine for preventing this disease and available drugs are not safe, understanding the mechanisms that regulate resistance and/or susceptibility to the disease could reveal novel targets for effective disease therapy and prevention. Thymic stromal lymphopoietin (TSLP) plays a critical role in driving Th2 immune response. Although susceptibility to experimental Trypanosoma congolense infection in mice is associated with excessive proinflammatory responses due in part to impaired Th2 response, the role of TSLP in resistance to African trypanosomiasis has not been well studied. Here, we investigated whether TSLP is critical for maintaining Th2 environment necessary for survival of T. congolense-infected mice. We observed an increased TSLP level in mice after infection with T. congolense, suggesting a role for this cytokine in resistance to the infection. Indeed, TSLPR-/- mice were more susceptible to T. congolense infection and died significantly earlier than their wild-type (WT) controls. Interestingly, serum levels of IFN-γ and TNF-α and the frequency of IFN-γ- and TNF-α-producing CD4+ T cells in the spleens and liver were significantly higher in infected TSLPR-/- mice than in the WT control mice. Susceptibility was also associated with excessive M1 macrophage activation. Treatment of TSLPR-/- mice with anti-IFN-γ mAb during infection abolished their enhanced susceptibility to T. congolense infection. Collectively, our study shows that TSLP plays a critical role in resistance to T. congolense infection by dampening the production of proinflammatory cytokines and its associated M1 macrophage activation.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TSLPHumansleeping sickness susceptibilityISOTslp (Mus musculus)protein:increased expression:serum (mouse)RGD 
TslpRatsleeping sickness susceptibilityISOTslp (Mus musculus)protein:increased expression:serum (mouse)RGD 
TslpMousesleeping sickness susceptibilityIEP protein:increased expression:serum (mouse)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tslp  (thymic stromal lymphopoietin)

Genes (Mus musculus)
Tslp  (thymic stromal lymphopoietin)

Genes (Homo sapiens)
TSLP  (thymic stromal lymphopoietin)


Additional Information