The immune response to Plasmodium chabaudi malaria in interleukin-4-deficient mice - PubMed (original) (raw)
. 1994 Oct;24(10):2285-93.
doi: 10.1002/eji.1830241004.
Affiliations
- PMID: 7925557
- DOI: 10.1002/eji.1830241004
The immune response to Plasmodium chabaudi malaria in interleukin-4-deficient mice
T von der Weid et al. Eur J Immunol. 1994 Oct.
Abstract
Interleukin(IL)-4 promotes the development of T helper (TH)2 cells, induces immunoglobulin class switching to IgG1 and is thought to be essential for switching to IgE. During a primary infection with the erythrocytic stages of Plasmodium chabaudi chabaudi, TH1 and TH2 cells specific for the parasite appear sequentially as infection progresses. To dissect the possible role of TH2 responses at the later stages of infection, mice with a targetted disruption of the IL-4 gene were infected with P. chabaudi. IL-4-deficient mice were able to control and clear a primary infection, although recrudescent parasitemias were significantly higher in these mice compared with wild-type littermates; demonstrating that IL-4 per se is not required for parasite elimination. To evaluate the actual impairment of TH2 functions in the absence of IL-4 in vivo during an infection with P. chabaudi; the cellular and humoral responses to the parasite generated in vitro and in vivo were compared in the two types of mice. Our data indicate that in vitro TH1 responses and ex vivo IL-12 mRNA levels were sustained in the IL-4-deficient mice compared with wild-type littermates. Correspondingly, TH2-associated cytokine mRNA such as IL-5 and IL-6, but not IL-10, were reduced early in infection in the deficient animals. However, these cytokines were expressed at comparable levels at the later stages of infection in both types of mice. Reflecting these differences in TH function, IgG1 responses were decreased in vitro and delayed in vivo, whereas IgG2a and IgG2b responses appeared earlier in vivo in the deficient mice. Strikingly, IgE secretion was not blocked in vivo in the deficient mice; the onset of the synthesis of IgE mRNA was delayed during infection and the amount of circulating IgE was five times lower than in the wild-type littermates after 5 weeks of infection. All these impairments of TH2-related activities were insufficient to affect parasite clearance in the deficient mice, probably due to the fact that such activities were only delayed and could take place normally at the later stages of infection.
Similar articles
- Possible modulation by male sex hormone of Th1/Th2 function in protection against Plasmodium chabaudi chabaudi AS infection in mice.
Zhang Z, Chen L, Saito S, Kanagawa O, Sendo F. Zhang Z, et al. Exp Parasitol. 2000 Nov;96(3):121-9. doi: 10.1006/expr.2000.4572. Exp Parasitol. 2000. PMID: 11162362 - Plasmodium chabaudi chabaudi: differential susceptibility of gene-targeted mice deficient in IL-10 to an erythrocytic-stage infection.
Linke A, Kühn R, Müller W, Honarvar N, Li C, Langhorne J. Linke A, et al. Exp Parasitol. 1996 Nov;84(2):253-63. doi: 10.1006/expr.1996.0111. Exp Parasitol. 1996. PMID: 8932775 - Dendritic cells, pro-inflammatory responses, and antigen presentation in a rodent malaria infection.
Langhorne J, Albano FR, Hensmann M, Sanni L, Cadman E, Voisine C, Sponaas AM. Langhorne J, et al. Immunol Rev. 2004 Oct;201:35-47. doi: 10.1111/j.0105-2896.2004.00182.x. Immunol Rev. 2004. PMID: 15361231 Review. - Selected problems of malaria blood stage immunity.
Perlmann P, Perlmann H, Berzins K, Troye-Blomberg M. Perlmann P, et al. Tokai J Exp Clin Med. 1998 Apr;23(2):55-62. Tokai J Exp Clin Med. 1998. PMID: 10021776 Review.
Cited by
- Interleukin-4 downregulates transcription factor BCL6 to promote memory B cell selection in germinal centers.
Shehata L, Thouvenel CD, Hondowicz BD, Pew LA, Pritchard GH, Rawlings DJ, Choi J, Pepper M. Shehata L, et al. Immunity. 2024 Apr 9;57(4):843-858.e5. doi: 10.1016/j.immuni.2024.02.018. Epub 2024 Mar 20. Immunity. 2024. PMID: 38513666 - Plasmodium berghei Hsp90 contains a natural immunogenic I-Ab-restricted antigen common to rodent and human Plasmodium species.
Enders MH, Bayarsaikhan G, Ghilas S, Chua YC, May R, de Menezes MN, Ge Z, Tan PS, Cozijnsen A, Mollard V, Yui K, McFadden GI, Lahoud MH, Caminschi I, Purcell AW, Schittenhelm RB, Beattie L, Heath WR, Fernandez-Ruiz D. Enders MH, et al. Curr Res Immunol. 2021 Jun 30;2:79-92. doi: 10.1016/j.crimmu.2021.06.002. eCollection 2021. Curr Res Immunol. 2021. PMID: 35492393 Free PMC article. - Investigating immune responses to parasites using transgenesis.
Tedla MG, Every AL, Scheerlinck JY. Tedla MG, et al. Parasit Vectors. 2019 Jun 15;12(1):303. doi: 10.1186/s13071-019-3550-4. Parasit Vectors. 2019. PMID: 31202271 Free PMC article. Review. - T cell-mediated immunity to malaria.
Kurup SP, Butler NS, Harty JT. Kurup SP, et al. Nat Rev Immunol. 2019 Jul;19(7):457-471. doi: 10.1038/s41577-019-0158-z. Nat Rev Immunol. 2019. PMID: 30940932 Free PMC article. Review. - γδ T cells modulate humoral immunity against Plasmodium berghei infection.
Inoue SI, Niikura M, Asahi H, Kawakami Y, Kobayashi F. Inoue SI, et al. Immunology. 2018 Dec;155(4):519-532. doi: 10.1111/imm.12997. Epub 2018 Sep 24. Immunology. 2018. PMID: 30144035 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical