Journal
IMMUNOLOGICAL REVIEWS
Volume 211, Issue -, Pages 8-22Publisher
WILEY
DOI: 10.1111/j.0105-2896.2006.00388.x
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL063925] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI046530] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [Z01AG000757, R37AG025805] Funding Source: NIH RePORTER
- Intramural NIH HHS [Z01 AG000757-10] Funding Source: Medline
- NHLBI NIH HHS [HL63925, P01 HL063925] Funding Source: Medline
- NIAID NIH HHS [AI021600, AI46530, P01 AI046530] Funding Source: Medline
- NIA NIH HHS [AG025805, R37 AG025805] Funding Source: Medline
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We have outlined the carefully orchestrated process of CD4(+) T-cell differentiation from naive to effector and from effector to memory cells with a focus on how these processes can be studied in vivo in responses to pathogen infection. We emphasize that the regulatory factors that determine the quality and quantity of the effector and memory cells generated include (i) the antigen dose during the initial T-cell interaction with antigen-presenting cells; (ii) the dose and duration of repeated interactions; and (iii) the milieu of inflammatory and growth cytokines that responding CD4(+) T cells encounter. We suggest that heterogeneity in these regulatory factors leads to the generation of a spectrum of effectors with different functional attributes. Furthermore, we suggest that it is the presence of effectors at different stages along a pathway of progressive linear differentiation that leads to a related spectrum of memory cells. Our studies particularly highlight the multifaceted roles of CD4(+) effector and memory T cells in protective responses to influenza infection and support the concept that efficient priming of CD4(+) T cells that react to shared influenza proteins could contribute greatly to vaccine strategies for influenza.
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