Jm. Penttila et al., EXPANSION OF A NOVEL PULMONARY CD3(-)CD4(-POPULATION IN MICE DURING CHLAMYDIA-PNEUMONIAE INFECTION() CD8(+) CELL), Infection and immunity, 66(7), 1998, pp. 3290-3294
A new pulmonary T-cell-like lymphocyte population with the phenotype C
D3(-) CD4(+) CD8(+) was discovered in mice. CD4(+) CD8(+) but CD3(+) c
ells among murine intestinal intraepithelial lymphocytes have previous
ly been described. We describe herein a dramatic expansion of the CD3(
-) CD4(+) CD8(+) cell population in response to experimental respirato
ry infection. After intranasal Chlamydia pneumoniae infection, CD3(+)
CD8(+) cells became transiently the dominant lymphocyte type (maximum
of 87% of all lymphocytes) in the lungs of NIH/S mice but remained vir
tually undetectable in spleen and blood. The enrichment of these cells
was not a C. pneumoniae-specific event, since infection of NIH/S mice
with influenza A virus also resulted in an increase in the number of
CD4(+) CD8(+) cells (maximum of 42% of all lymphocytes). In addition t
o outbred NIH/S mice, two other mouse strains were studied: BALB/c (H-
2(d)) and C57BL/6 (H-2(b)). C. pneumoniae-infected BALB/c mice respond
ed with an intermediate increase in the number of CD4(+) CD8(+) cells
in lungs, whereas C57BL/6 mice did not respond. The double-positive CD
4(+) CD8(+) cells lacked a major part of the T-cell receptor complex,
being both CD3(-) and TCR alpha beta(-). However, when they were stimu
lated in vitro with a T-cell mitogen, they responded by proliferation
but did not secrete gamma interferon, The dramatic expansion of this c
ell population at the infection site suggests an active role for them
in respiratory infection, but the specification of this requires furth
er study.