Bovine monocytes induce immunoglobulin production in peripheral blood B lymphocytes.

Although a role for monocytes and monocyte-derived dendritic cells (DC) in the activation of T cells is well established, it is less clear to what extent DC and their precursors, monocytes, regulate B cell immune responses. Here we show that regulatory mechanisms similar to those in humans are in place in the bovine immune system. In vitro culture of bovine monocytes with bovine B cells activated by the anti-CD3 triggered CD4+ T cells or through immunoglobulin (Ig) receptor crosslinking induces B cell Ig secretion. Unlike bovine monocyte-derived DC, monocytes do not promote Ig class switching to IgG and IgA in activated peripheral blood B cells. These results suggest that bovine monocytes are capable of directly inducing Ig secretion in activated bovine peripheral blood B cells, but do not provide the signals for B cell Ig class switching.

Bovine dendritic cells generated from monocytes and bone marrow progenitors regulate immunoglobulin production in peripheral blood B cells.

We examined whether bovine monocyte-derived and bone marrow (BM) dendritic cells (DCs) regulate antibody production in activated peripheral blood B cells. DCs were generated from monocytes and BM progenitors in the presence of bovine recombinant granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4). Monocyte-derived DCs promoted B cells activated by the anti-CD3 triggered CD4(+) T cells or through immunoglobulin M (IgM) receptor to increase the level of IgG secretion. Furthermore, the addition of DCs triggered B cells activated through IgM receptors to produce IgG2 and IgA, thus inducing an isotype switch. BM-derived DCs increased the production of IgG in B cells activated by the anti-CD3 triggered CD4(+) T cells, but unlike monocyte-derived DCs did not have any effect on B cells activated through surface IgM. These data suggest that the regulation of humoral immune responses in cattle depends on the origin of DCs and the mode of B cell activation.

Recurrence of unilateral retinoblastoma following radiation therapy.

A retrospective analysis of 65 unilateral retinoblastoma patients treated initially with external beam radiation, revealed that 25 eyes (38.5%) developed local recurrence of retinoblastoma. The mean age at diagnosis was 1.8 years for patients who developed recurrences vs. 0.9 years for those who did not. Ninety-six percent of the recurrences occurred less than two years from the age at diagnosis; the amount of time from the end of external beam radiation treatment until a tumor recurred was independent of the age at diagnosis. The initial largest basal diameter was 10.7 DD for tumors which later recurred and 5.9 DD for tumors that were cured. Sixty-nine percent of eyes in groups III-V had tumor recurrence, and 10% of eyes in groups I-II had recurrence. All but one eye (24 eyes) that developed recurrence were enucleated. Family history of retinoblastoma, location of the tumor, gender, and laterality did not significantly correlate with the mean age of initial diagnosis for tumors that recurred or the mean time of onset for recurrence.

Unilateral retinoblastoma: new intraocular tumours after treatment.

A retrospective chart review of 427 eyes diagnosed with unilateral retinoblastoma was performed to determine which eyes, which patients, and when new intraocular tumours would develop after treatment. Mean follow up was 8.16 years. Twenty five (6%) of 427 unilateral retinoblastoma patients developed new intraocular tumours after treatment. Five (1%) unilateral patients who were previously treated with enucleation developed new tumours (in the fellow eye). Fifteen (24%) unilateral patients who were previously treated with external beam radiation developed new tumours (equally in either eye). New tumours did not develop in the macula of either eye. The relative risk of developing new intraocular tumours after treatment was 16% in patients diagnosed before 1 year old and 2.2% for patients diagnosed after 1 year old (p < 0.001). The mean time to onset for the development of new tumours after treatment was 0.74 years; no new tumours appeared after 7.5 years of age. Those patients who are diagnosed with unilateral retinoblastoma in the first 6 months of life and have a family history of the disease are at greatest risk of developing new intraocular tumours.