EFFECTS OF INVIVO DEPLETION OF IMMUNOCYTE POPULATIONS ON HERPES-SIMPLEX VIRUS GLYCOPROTEIN-D VACCINE-INDUCED RESISTANCE TO HSV2 CHALLENGE
VIRAL IMMUNOLOGY
Authors: MISHKIN, EM; BLASIAK, M; GIORGIO, D; ISHIZAKA, ST
Abstract
BALB/c mice, preimmunized with a protective dose of native herpes simplex virus type 1 glycoprotein D (ngD1) vaccine, were depleted of selected immunocyte populations in vivo using monoclonal antibodies directed at Thy1+, L3T4+, or Lyt2+ cells. Following immunization and depletion, animals were inoculated with varied challenge levels of herpes simplex virus type 2 (HSV2) in the footpad and were monitored for disease. Both depleted and undepleted gD-immunized mice were significantly protected when compared with placebo controls. T-cell-independent protection in Thy1 and L3T4-depleted ngD1-immunized animals was effective at low and moderate levels of HSV2 challenge levels, high levels of HSV2 giving high symptom scores in immunized and depleted mice. Depletion of Lyt2+ cells had no significant effect on the outcome of HSV2 infection. Depleted and nondepleted animals also were assessed in parallel for cellular and humoral responsiveness to ngD1 and to HSV antigens in vitro. Lymphoproliferative responses were abrogated in gD-immunized mice treated with anti-Thy1 or anti-L3T4, anti-Lyt2 treatment having little effect. Postimmunization T-cell depletion did not undermine ELISA or neutralizing antibody responses. These findings suggest that at low to moderate levels of virus challenge vaccine-elicited antibody plays a primary role in limiting the severity of infection, T-cell-mediated protective responses being of enhanced significance only at high levels of virus challenge.
Chlamydia psittaci is variably associated with ocular adnexal MALT lymphoma in different geographical regions
JOURNAL OF PATHOLOGY
Authors: Chanudet, E.; Zhou, Y.; Bacon, C. M.; Wotherspoon, A. C.; Mueller-Hermelink, H.-K.; Adam, P.; Dong, H. Y.; de Jong, D.; Li, Y.; Wei, R.; Gong, X.; Wu, Q.; Ranaldi, R.; Goteri, G.; Pileri, S. A.; Ye, H.; Hamoudi, R. A.; Liu, H.; Radford, J.; Du, M-Q
Abstract
Infectious agents play a critical role in MALT lymphoma development. Studies from Italy showed Chlamydia psittaci infection in 87% of ocular adnexal MALT lymphomas and complete or partial regression of the lymphoma after C psittaci eradication in four of nine cases. However, C. psittaci was not demonstrated in ocular adnexal MALT lymphomas from the USA. This study was thus designed to investigate further the role of C psittaci, and other infectious agents commonly associated with chronic eye disease, in the development of ocular adnexal MALT lymphoma. The presence of C psittaci, C trachomatis, C pneumoniae, herpes simplex virus 1 and 2 (HSV1, HSV2), and adenovirus 8 and 19 (ADV8, ADV19) was assessed separately by polymerase chain reaction in 142 ocular adnexal MALT lymphomas, 53 non-marginal zone lymphomas, and 51 ocular adnexal biopsies without a lymphoproliferative disorder (LPD), from six geographical regions. C psittaci was detected at similar low frequencies in non-LPD and non-marginal zone lymphoma groups from different geographical regions (0-14%). Overall, the prevalence of C psittaci was significantly higher in MALT lymphomas (22%) than in non-LPD (10%, p = 0.042) and non-marginal zone lymphoma cases (9%, p = 0.033). However, the prevalence of C. psittaci infection in MALT lymphoma showed marked variation among the six geographical regions examined, being most frequent in Germany (47%), followed by the East Coast of the USA (35%) and the Netherlands (29%), but relatively low in Italy (13%), the UK (12%), and Southern China (11%). No significant differences in the detection of C. pneumoniae, C trachomatis, HSV1, HSV2, ADV8, and ADV19 were found between lymphomas and controls from different geographical regions. In conclusion, our results show that C psittaci, but not C. pneumoniae, C. trachomatis, HSV1, HSV2, ADV8 or ADV19, is associated with ocular adnexal MALT lymphoma and that this association is variable in different geographical areas. Copyright (c) 2006 Pathological Society of Great Britain and Ireland.