scholarly journals Imiquimod Does not Affect Shedding of Viable Chlamydiae in a Murine Model ofChlamydia trachomatisGenital Tract Infection

2003 ◽  
Vol 11 (2) ◽  
pp. 81-87 ◽  
Author(s):  
Kyle H. Ramsey ◽  
Namir Shaba ◽  
Kevin P. Cohoon ◽  
Kevin A. Ault
Keyword(s):  
Immune Response ◽  
Murine Model ◽  
Antibody Responses ◽  
Igg Subclass ◽  
T Helper ◽  
Type 2 Immune Response ◽  
Significant Difference ◽  
Helper Type

Objective:We postulated that either oral or vaginal administration of the immune response modifier imiquimod would decrease vaginal shedding ofChlamydia trachomatis, mouse pneumonitis strain (MoPn), in a murine model.Methods:Female BALB/c mice were infected intravaginally withC. trachomatis(MoPn) and were administered imiquimod either orally (30 mg/kg) or vaginally (10 μl of 5%imiquimod cream) prior to infection and every second day after infection for a total of four doses. The course of infection was monitored by collecting cervical–vaginal swabs and isolation in HeLa 229 cell culture. To determine whether the drug affected T helper type 1 or T helper type 2 immune response polarization, immunoglobulinG(IgG) subclass antibody responses were assessed at day 56 after infection.Results:There was no significant difference in the course of infection when imiquimod-treated mice were compared with sham-treated controls, regardless of whether the drug was administered orally or vaginally. IgG subclass antibody responses, and by extension, T helper type 1 to T helper type 2 immune response polarization, were also unaffected.Conclusions:Imiquimod has no efficacy in controllingC. trachomatis(MoPn) infection in the murine model.

scholarly journals Natural killer T cells are required for the development of a superantigen-driven T helper type 2 immune response in mice

Immunology ◽  
2005 ◽  
Vol 116 (2) ◽  
pp. 233-244 ◽  
Author(s):  
Auro Nomizo ◽  
Edilberto Postol ◽  
Raquel de Alencar ◽  
Fabiola Cardillo ◽  
Jose Mengel
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Natural Killer ◽  
Natural Killer T Cells ◽  
T Helper ◽  
Type 2 Immune Response ◽  
Killer T Cells ◽  
Helper Type ◽  
Natural Killer T

Regulation of the immune response by nitric oxide differentially produced by T helper type 1 and T helper type 2 cells

1994 ◽  
Vol 24 (4) ◽  
pp. 980-984 ◽  
Author(s):  
Andrew W. Taylor-Robinson ◽  
Foo Y. Liew ◽  
Alison Severn ◽  
Damo Xu ◽  
Stephen J. McSorley ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Immune Response ◽  
T Helper ◽  
Helper Type

scholarly journals IL-4–producing B cells regulate T helper cell dichotomy in type 1- and type 2-controlled diseases

2017 ◽  
Vol 114 (40) ◽  
pp. E8430-E8439 ◽  
Author(s):  
Ramona Hurdayal ◽  
Hlumani H. Ndlovu ◽  
Mélanie Revaz-Breton ◽  
Suraj P. Parihar ◽  
Justin Komguep Nono ◽  
...  
Keyword(s):  
Immune Response ◽  
B Cells ◽  
B Cell ◽  
Cutaneous Leishmaniasis ◽  
Leishmania Major ◽  
Interleukin 4 ◽  
T Helper ◽  
Type 2 Immune Response

Interleukin-4 (IL-4)–induced T helper (Th) 2 cells promote susceptibility to the protozoan parasite Leishmania major, while conferring immunity to the intestinal trematode Schistosoma mansoni. Here, we report that abrogation of IL-4 receptor alpha (IL-4Rα) signaling on B cells in BALB/c mice (mb1creIL-4Rα–/lox) transformed nonhealer BALB/c to a healer phenotype with an early type 1 and dramatically reduced type 2 immune response and an absence of ulceration and necrosis during cutaneous leishmaniasis. From adoptive reconstitution and mixed bone-marrow chimera studies in B cell-deficient (µMT) mice, we reveal a central role for B cell-derived IL-4 and IL-4Rα in the optimal induction of the susceptible type 2 phenotype to L. major infection. We further demonstrate that the absence of IL-4Rα signaling on B cells exacerbated S. mansoni-induced mortality and pathology in BALB/c mice, due to a diminished type 2 immune response. In both disease models, IL-4Rα–responsive B cells displayed increased IL-4 production as early as day 1 after infection. Together, these results demonstrate that IL-4–producing and IL-4Rα–responsive B cells are critical in regulating and assisting early T helper dichotomy toward Th2 responses, which are detrimental in cutaneous leishmaniasis but beneficial in acute schistosomiasis.

PS3-02 Neutralization of endogenous IL-12 inhibits the T-helper Type 1 immune response in experimental Sporothrix SchenckII infection

Cytokine ◽  
2010 ◽  
Vol 52 (1-2) ◽  
pp. 82
Author(s):  
Aurelio Flores-Garcı´a ◽  
Vicente Garibaldi-Becerra ◽  
Martha Barba-Barajas ◽  
Jesus S. Velarde-Félix ◽  
Luis E. Wong-Ley-Madero ◽  
...  
Keyword(s):  
Immune Response ◽  
Sporothrix Schenckii ◽  
T Helper ◽  
Helper Type

scholarly journals Implications of pre-existing asthma on COVID-19 pathogenesis

2021 ◽  
Author(s):  
Rakhee K. Ramakrishnan ◽  
Saba Al Heialy ◽  
Qutayba Hamid
Keyword(s):  
Severe Disease ◽  
Current Data ◽  
Public Healthcare ◽  
T Helper ◽  
The Public ◽  
Type 2 Immune Response ◽  
Asthma Patients ◽  
Common Respiratory Virus ◽  
Helper Type

The coronavirus disease 2019 (COVID-19) pandemic spreading at an alarming rate has taken a heavy toll on the public healthcare systems and economies worldwide. An abnormal and overactivated inflammatory response is occasionally elicited by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and this hyperinflammation is associated with worse prognosis of COVID-19. Theoretically, one would expect asthma patients to be at a greater risk of SARS-CoV-2 infection considering their increased susceptibility to common respiratory virus-associated exacerbations. Surprisingly, current data do not consistently suggest an increased prevalence of asthma among COVID-19 patients. Considering the high global prevalence of asthma, the characteristics of the disease and/or their conventional therapy might play a role in their potential defense against COVID-19. This may be attributed to the T helper type 2 immune response predominantly seen in asthmatics. Likewise, asthma therapeutics, including corticosteroids and biologics, may in fact benefit the asthmatics by alleviating the development of hyperinflammation. On the other hand, elevated IL-17 levels are characteristically seen in a subset of asthma patients with severe disease as well as in COVID-19 patients. Targeting the IL-17 pathway as a treatment strategy could plausibly alleviate acute respiratory distress syndrome (ARDS) in COVID-19 patients with asthma demonstrating a predominant T helper type 17 response. A clinical trial including a drug targeting this pathway may thus, constitute a logical addition to the global pursuit for effective therapeutics against COVID-19. The complex interplay between the asthma endotypes and COVID-19 is not very well understood and will be discussed in this mini-review.

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