Table 3. Number of CD11b⁺CD11c^Hi and CD11b⁺CD11c^Lo cells 14 days after pneumococcal challenge.

		IL-10	IFN-γ	CCR5
Spleen	CD11b+CD11cHi Control Ab	2.32 ± 0.2	3.73 ± 0.2	19.6 ± 0.1
	CD11b+CD11c Hi Anti-CCL5 Ab	4.41 ± 0.2*	2.57 ± 0.3*	12.5 ± 0.2*
Cervical Lymph Node	CD11b+CD11c Hi Control Ab	0.10 ± 0.1	0.29±0.1	1.66 ± 0.1
	CD11b+CD11c Hi Anti-CCL5 Ab	0.21 ± 0.2*	0.11 ± 0.1*	1.58 ± 0.2
Spleen	CD11b+CD11cLo Control Ab	8.85 ± 0.3	7.68 ± 0.3	7.56 ± 0.1
	CD11b+CD11c Lo Anti-CCL5 Ab	10.4 ± 0.2	8.62 ± 0.3	6.09 ± 0.1
Cervical Lymph Node	CD11b+CD11c Lo Control Ab	0.18 ± 0.1	0.40 ± 0.1	0.99 ± 0.2
	CD11b+CD11c Lo Anti-CCL5 Ab	0.22 ± 0.1	0.73±0.2*	0.77 ± 0.1

C57BL/6 × BALB/c F1 mice were intranasally challenged with PBS (uninfected) or 10⁷ CFUs of S. pneumoniae strain EF3030 in a 15 μL volume of Ringer’s solution and treated with either control or anti-CCL5 antibodies. Spleen and cervical lymph node lymphocytes were purified and prepared for cell surface and intracellular flow cytometry analysis 14 days after bacterial challenge. The fold increases ± SEM in the number of (×10⁶) of CD3⁻CD11b⁺ CD11c^Hi or CD3⁻ CD11b⁺ CD11c^Lo lymphocytes that were CCL5, IL-10, IFN-γ or CCR5 positive are shown. Asterisks (*) indicate statistically significant (p < 0.01) increases between infected over infected local cell subpopulations from three separate experiments with two groups containing 10 mice each.