Natural killer cells regulate T-cell proliferation during human parainfluenza virus type 3 infection.
Human parainfluenza virus type 3 (HPIV3) is a major respiratory pathogen in humans. Failure to induce immunological memory associated with HPIV3 infection has been attributed to inhibition of lymphocyte proliferation. We demonstrate that the inability of mixed lymphocytes to respond to virally infected antigen-presenting cells is due to an interleukin-2-dependent, nonapoptotic mechanism involving natural killer (NK) cells and their influence is exerted in a contact-dependent manner. These results suggest a novel regulatory mechanism for NK cells during HPIV3 infection, offering an explanation for viral persistence and poor memory responses.
Noone
Cariosa M
CM
Viral Immunology laboratory, School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland.
Paget
Elaine
E
Lewis
Ellen A
EA
Loetscher
Marius R
MR
Newman
Robert W
RW
Johnson
Patricia A
PA
D000938:Antigen-Presenting Cells / Q000276:immunology*; D017252:CD3 Complex / Q000378:metabolism; D002478:Cells, Cultured; D018920:Coculture Techniques; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology*; D010224:Parainfluenza Virus 3, Human / Q000276:immunology / Q000472:pathogenicity*; D010253:Respirovirus Infections / Q000276:immunology* / Q000821:virology; D013601:T-Lymphocytes / Q000276:immunology*
D017252:CD3 Complex; D007376:Interleukin-2