Campbell, Sharon M. and Knipper, Johanna A. and Ruckerl, Dominik and Finlay, Conor M. and Logan, Nicola and Minutti, Carlos M. and Mack, Matthias and Jenkins, Stephen J. and Taylor, Matthew D. and Allen, Judith E. (2018) Myeloid cell recruitment versus local proliferation differentiates susceptibility from resistance to filarial infection. ELIFE, 7: e30947. ISSN 2050-084X,
Full text not available from this repository. (Request a copy)Abstract
Both T(H)2-dependent helminth killing and suppression of the T(H)2 effector response have been attributed to macrophages (M Phi) activated by IL-4 (M(IL-4)). To investigate how M(IL-4) contribute to diverse infection outcomes, the MO compartment of susceptible BALB/c mice and more resistant C57BL/6 mice was profiled during infection of the pleural cavity with the filarial nematode, Litomosoides sigmodontis. C57BL/6 mice exhibited a profoundly expanded resident M Phi(resM Phi) population, which was gradually replenished from the bone marrow in an age dependent manner. Infection status did not alter the bone-marrow derived contribution to the resM Phi population, confirming local proliferation as the driver of resM Phi expansion. Significantly less resM Phi expansion was observed in the susceptible BALB/c strain, which instead exhibited an influx of monocytes that assumed an immunosuppressive PD-L2(+) phenotype. Inhibition of monocyte recruitment enhanced nematode killing. Thus, the balance of monocytic vs. resident M(IL-4) numbers varies between inbred mouse strains and impacts infection outcome.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ALTERNATIVELY ACTIVATED MACROPHAGES; TISSUE-RESIDENT MACROPHAGES; LITOMOSOIDES-SIGMODONTIS; REVEALS; IGM; INTERLEUKIN-4; POLARIZATION; PROTECTION; MONOCYTES; MICE; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 23 Mar 2020 11:08 |
| Last Modified: | 23 Mar 2020 11:08 |
| URI: | https://pred.uni-regensburg.de/id/eprint/15218 |
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