Impaired in vitro T-cell responses in patients with community acquired pneumonia.

To evaluate the status of the cellular immune response of patients with community acquired pneumonia (CAP), 8 CAP cases were studied for their in vitro T-cell responses to concanavalin A (Con A), tuberculin, and candidin, as well as levels of major T-cell populations in peripheral blood. Assessment on admission revealed that CAP patients had significantly decreased responses to both antigen and mitogen driven lymphocyte proliferation when compared to age and sex matched controls. Studies performed upon 1 week of antibiotic treatment made evident, in turn, that clinical improvement was accompanied by a reestablishment of the in vitro responses to tuberculin and candidin, whereas the lymphoproliferation induced by Con A remained decreased as in its first evaluation. Data from admission and day 7 of treatment showed no significant differences as to the levels of peripheral T-cell subsets when compared to those of healthy controls. Our results indicate that CAP coincides with reduced in vitro T-cell responses to antigen and mitogen stimulation.

[Concomitant immunity against Sarcoma E 100 comparing 2 strains of rats]. / Inmunidad concomitante contra el Sarcoma E 100 comparando dos líneas de ratas.

Concomitant immunity (IC) is usually defined as the capacity of any animal bearing a progressor tumor to inhibit a second challenge with the same tumor. In order to establish the contribution of the host to the origin of this phenomenon, IC was induced in two lines of rats with a different behavior when challenged with Sarcoma E 100 (SE 100), i.e., line IIMc: 90% take and 100% regression; line "m": 100% take and death. The rats received a second challenge on day 3 (Group II), 7 (III), and 14 (IV), as well as the control groups: II', III' and IV', respectively. The animals reinoculated on day 7 showed a decrease, both in percentage of takes (Fig. 1, III vs III') and tumor surface (Table 1, 2). Likewise, in rats IIMc, a lesser development of the first inoculum (Table 1, Ia vs I') was observed. The Winn assay (Table 3) confirmed the presence of immunocompetent spleen cells (CE) against SE 100 in IIMc rat spleens: namely, 1) immune rats (II), 2) unique tumor bearing rats (IV), 3) first progressor and second negative inoculum (V). In line "m" the percentage of takes was only smaller in the group inoculated conjointly with CE from immune rats (Table 3, VI vs VII). A mere 10% (3/30) of "m" rats were immunized against SE 100. Consequently, these results could attribute the IC, in IIMc rats, to immunological mechanisms, while in "m" it could be due to factor(s) released and/or induced by the first tumor, as proposed by Gorelik.

Inmunidad concomitante contra el Sarcoma E 100 comparando dos líneas de ratas. / [Concomitant immunity against Sarcoma E 100 comparing 2 strains of rats]

Concomitant immunity (IC) is usually defined as the capacity of any animal bearing a progressor tumor to inhibit a second challenge with the same tumor. In order to establish the contribution of the host to the origin of this phenomenon, IC was induced in two lines of rats with a different behavior when challenged with Sarcoma E 100 (SE 100), i.e., line IIMc: 90

take and 100

regression; line [quot ]m[quot ]: 100

take and death. The rats received a second challenge on day 3 (Group II), 7 (III), and 14 (IV), as well as the control groups: II, III and IV, respectively. The animals reinoculated on day 7 showed a decrease, both in percentage of takes (Fig. 1, III vs III) and tumor surface (Table 1, 2). Likewise, in rats IIMc, a lesser development of the first inoculum (Table 1, Ia vs I) was observed. The Winn assay (Table 3) confirmed the presence of immunocompetent spleen cells (CE) against SE 100 in IIMc rat spleens: namely, 1) immune rats (II), 2) unique tumor bearing rats (IV), 3) first progressor and second negative inoculum (V). In line [quot ]m[quot ] the percentage of takes was only smaller in the group inoculated conjointly with CE from immune rats (Table 3, VI vs VII). A mere 10

(3/30) of [quot ]m[quot ] rats were immunized against SE 100. Consequently, these results could attribute the IC, in IIMc rats, to immunological mechanisms, while in [quot ]m[quot ] it could be due to factor(s) released and/or induced by the first tumor, as proposed by Gorelik.

[Effect of intratumor macrophages on the growth of a rat sarcoma]. / Influencia de los macrófagos intratumorales en el crecimiento de un sarcoma de rata.

The removal of active phagocytic cells (CFA) from suspensions of a rat sarcoma (S-E 100) caused a decrease in tumor development in "m" line rats; consequently, we postulated that the macrophage (M phi) population infiltrating the tumor might possess inhibitory functions. In the present paper we investigate whether the effect of CFA is a general one or whether it is dependent on the interaction between M phi infiltrating the tumor and the recipient. S-E 100 was inoculated in "m" line rats (S-E 100,m) and in "c" (S-E 100,c); CFA were depleted from both tumoral suspensions with carbonyl iron powder (FeC), inoculating the supernatant tumor sells denominated S.FeC-m and S.FeC-c, and the corresponding control suspensions, S Te-m and S Te-c. Inocula for both recipients were subcutaneous and contained 1 x 10(6) cells. The elimination of CFA induced a decrease in the development of the tumor in "m" recipients only when the inoculum was provided by S-E 100, m (Table 1). On the contrary no change in tumor growth was detected in the "C" recipients, whether the inoculum was provided by SE-100, m or by S-E 100, c (Table 1). An inhibitory effect on the immune response exerted by M phi infiltrating S-E 100, as a non general effect, is postulated. This effect was obtained only when intratumoral M phi were syngeneic with the recipient and specifically for "m" line.

Influencia de los macrófagos intratumorales en el crecimiento de un sarcoma de rata. / [Effect of intratumor macrophages on the growth of a rat sarcoma]

The removal of active phagocytic cells (CFA) from suspensions of a rat sarcoma (S-E 100) caused a decrease in tumor development in [quot ]m[quot ] line rats; consequently, we postulated that the macrophage (M phi) population infiltrating the tumor might possess inhibitory functions. In the present paper we investigate whether the effect of CFA is a general one or whether it is dependent on the interaction between M phi infiltrating the tumor and the recipient. S-E 100 was inoculated in [quot ]m[quot ] line rats (S-E 100,m) and in [quot ]c[quot ] (S-E 100,c); CFA were depleted from both tumoral suspensions with carbonyl iron powder (FeC), inoculating the supernatant tumor sells denominated S.FeC-m and S.FeC-c, and the corresponding control suspensions, S Te-m and S Te-c. Inocula for both recipients were subcutaneous and contained 1 x 10(6) cells. The elimination of CFA induced a decrease in the development of the tumor in [quot ]m[quot ] recipients only when the inoculum was provided by S-E 100, m (Table 1). On the contrary no change in tumor growth was detected in the [quot ]C[quot ] recipients, whether the inoculum was provided by SE-100, m or by S-E 100, c (Table 1). An inhibitory effect on the immune response exerted by M phi infiltrating S-E 100, as a non general effect, is postulated. This effect was obtained only when intratumoral M phi were syngeneic with the recipient and specifically for [quot ]m[quot ] line.