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In malaria endemic countries, this immunological balance may be influenced by micronutrient deficiencies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Peripheral blood mononuclear cells from Tanzanian preschool children were stimulated<jats:italic>in vitro<\/jats:italic>with<jats:italic>Plasmodium falciparum<\/jats:italic>-parasitized red blood cells to determine T-cell responses to malaria under different conditions of nutrient deficiencies and malaria status.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The data obtained indicate that zinc deficiency is associated with an increase in TNF response by 37%; 95% CI: 14% to 118% and IFN-\u03b3 response by 74%; 95% CI: 24% to 297%. Magnesium deficiency, on the other hand, was associated with an increase in production of IL-13 by 80%; 95% CI: 31% to 371% and a reduction in IFN-\u03b3 production. These results reflect a shift in cytokine profile to a more type I cytokine profile and cell-cell mediated responses in zinc deficiency and a type II response in magnesium deficiency. The data also reveal a non-specific decrease in cytokine production in children due to iron deficiency anaemia that is largely associated with malaria infection status.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The pathological sequels of malaria potentially depend more on the balance between type I and type II cytokine responses than on absolute suppression of these cytokines and this balance may be influenced by a combination of micronutrient deficiencies and malaria status.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1475-2875-9-162","type":"journal-article","created":{"date-parts":[[2010,6,15]],"date-time":"2010-06-15T06:15:18Z","timestamp":1276582518000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Effect of nutrient deficiencies on in vitro Th1 and Th2 cytokine response of peripheral blood mononuclear cells to Plasmodium falciparum infection"],"prefix":"10.1186","volume":"9","author":[{"given":"Erasto V","family":"Mbugi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marjolein","family":"Meijerink","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacobien","family":"Veenemans","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prescilla V","family":"Jeurink","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew","family":"McCall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raimos M","family":"Olomi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John F","family":"Shao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaffu O","family":"Chilongola","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans","family":"Verhoef","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huub FJ","family":"Savelkoul","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2010,6,14]]},"reference":[{"key":"1243_CR1","doi-asserted-by":"publisher","first-page":"13","DOI":"10.1126\/science.298.5591.13","volume":"298","author":"KS Aultman","year":"2002","unstructured":"Aultman KS, Gottlieb M, Giovanni MY, Fauci AS: Editorial: Anopheles gambiae genome: completing the malaria triad. 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