
doi: 10.1038/eye.1994.3
pmid: 8013704
The immune defence against herpes virus in keratitis requires an intricate interplay of macrophages, B-lympho cytes, cytotoxic Tand helper T-lymphocytes, sometimes by direct contact, sometimes by exchange of mediators. In most diseases immunological interactions take place in lymphoid organs, where lymphocytes, macrophages and other cells are tightly packed in great numbers, facilitating the exchanges. This is the site where the first encounter with herpes virus leads to immunisation. However, in I clinical practice we usually treat dendritic keratitis in adults who have already been immunised to herpes virus, a long time ago. Specific lymphocytes have already been activated previously, they have moved out of the lymph nodes and are present as memory cells in all tissues. There are many good arguments to support the view that in keratitis the immune response to this new challenge occurs in the ocular tissues, in full view of the biomicro scope, and not in distant lymph nodes. Although the opti cal resolution of a slit lamp is insufficient for a detailed observation of leucocytes, a skilled ophthalmologist is able to recognise their presence and activity. The immune defences rest primarily on the action of a few classes of specialised cells, among them the B-lym phocytes and the T-Iymphocytes.
Adult, B-Lymphocytes, Immunity, Cellular, T-Lymphocytes, Endothelium, Corneal, Immunoglobulins, Herpesvirus 1, Human, Keratitis, Dendritic, Mice, Keratitis, Herpetic, Animals, Humans, Female, Rabbits
Adult, B-Lymphocytes, Immunity, Cellular, T-Lymphocytes, Endothelium, Corneal, Immunoglobulins, Herpesvirus 1, Human, Keratitis, Dendritic, Mice, Keratitis, Herpetic, Animals, Humans, Female, Rabbits
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