Papel de los linfocitos t cd4+ y cd8+ en la protección inducida por diferentes vacunas contra chlamydophila abortus

  1. Ortega Hernández, Nieves
  2. Caro Vergara, María Rosa
  3. Salinas Lorente, Jesús
Journal:
Anales de veterinaria de Murcia

ISSN: 0213-5434 1989-1784

Year of publication: 2006

Issue: 22

Pages: 25-34

Type: Article

More publications in: Anales de veterinaria de Murcia

Abstract

Chlamydophila abortus is the etiological agent of ovine enzootic abortion (OEA). For the control of this disease there are two types of commercially available vaccines: inactivated vaccines and attenuated vaccines. Previous studies have demonstrated that an effective vaccine against C. abortus must induce a Th1 immune response involving an early IFN-ã production and CD8+ T cells activation. The aim of the present work was to clarify, using a mouse model, the role of CD4+ and CD8+ T lymphocytes in the establishment of a protective immune response against C. abortus infection in mice previously vaccinated. Mice were vaccinated with a commercially available vaccine (1B) and two experimental inactivated vaccines. The inactivated vaccines were adjuvated with aluminium hydroxide (HA) or QS-21 (QS) respectively. After vaccination and few days before the challenge, mice were depleted of CD4+ and CD8+ T cells using monoclonal antibodies produced by GK 1.5 (anti-CD4) and 2.43 (anti-CD8) hybridome cells. In depleted CD4+ T cells mice, morbidity and mortality results showed lower weight lost in HA and 1B vaccinated mice at day 4 p.i. while none of infected mice died. In depleted CD8+ T cells mice, no mortality was observe in vaccinated mice while 75% of control non vaccinated mice succumbed to C. abortus infection at day 8 p.i. The bacterium isolation results showed an increase clamidial burden in liver in both depletion experiments associated with a slower infection resolution. Thus, in vaccinated mice the absence of any of the two lymphocyte T cells subpopulation (CD4+ or CD8+) in not essential per se in the establishment of a protective immune response during the infection.