PubMed · 1979 · 55 citations · 11 references
Life SciencesEntomologyImmunologyDermatopathologyImmunopathologyInnate ImmunityComplement SystemImmunopathology Of SkinTick BiologyTick-associated Skin DiseaseTick-borne DiseasesTick-borne Parasitic DiseasesAntigen-antibody InteractionsAntigen-antibody RecognitionComplement Activation PathwaysEpidermal HistologyLangerhans Cell FunctionTick Attachment Site LesionsTick ImmunobiologyTick-associated Cutaneous Lesions
Using indirect immunoflorescence techniques, tick salivary gland antigens (SGA) were demonstrable in cement deposited on the skin by ticks and in all layers of the epidermis of infested guinea-pigs close to the sites where ticks attached. The antigen remained in these sites for several days after ticks had detached. In tick-resistant but not in normal guinea-pigs, SGA, complement and IgG were deposited at the dermo-epidermal junction even at some distance from the attachment site. Complement was also demonstrable in epidermal vesicles which developed beneath larvae attached to resistant guinea-pigs. It is suggested that antigen-antibody reaction and complement activation at these sites may play a role in the development of skin lesions and the attraction of basophils to these areas in challenged tick-resistant guinea-pigs. Tick antigens were also found to be associated with dendritic suprabasal cells in the epidermis of resistant guinea-pigs. It has previously been proposed that such SGA-trapping cells are Langerhans cells. These cells, in the presence of specific antibody and complement, could also initiate epidermal lesions in resistant guinea-pigs.
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Acquired resistance to ticks. I. Passive transfer of resistance.
Stephen K. Wikel, John R. Allen · PubMed · 1976 · 122 citations
Acquired resistance to ticks. III. Cobra venom factor and the resistance response.