A corneal cytokine triggers the in vivo synthesis of serum amyloid A by hepatocytes.

Recently a cytokine released by primary corneal epithelial cell cultures as well as by a rabbit corneal cell line (SIRC), corneal epithelial cell-derived thymocyte-activating factor (CETAF) has been described. The biological and biochemical properties of CETAF are similar to those of epidermal cell-derived factor (ETAF) and macrophage-derived interleukin 1 (IL 1). Like IL 1 or ETAF, SIRC supernatant, as well as partially purified CETAF (both molecular weight pools) significantly enhanced serum amyloid A production by hepatocytes, when injected intraperitoneally into C3H/HeJ mice.

An epidermal cell-derived cytokine triggers the in vivo synthesis of serum amyloid A by hepatocytes.

Lipopolysaccharide (LPS) stimulates macrophages to produce a number of closely related soluble mediators, including interleukin 1 (IL 1), endogenous pyrogen (EP), and serum amyloid A (SAA) inducer, which are able to induce hepatocyte production of SAA, an acute-phase reactant. Keratinocytes also produce a soluble mediator, epidermal cell-derived thymocyte-activating factor (ETAF), which is very similar to IL 1. The experiments reported here show that unpurified ETAF-containing preparations, as well as ETAF after chromatography by gel filtration (Sephacryl S-200), anion-exchange on DEAE, phenyl-Sepharose, or isoelectrofocusing, were all able to induce the in vivo production of SAA by hepatocytes.

Antigens of the basement membranes of the seminiferous tubules induce autoimmunity in Wistar rats.

A preparation enriched in basement membranes from seminiferous tubules was isolated from rat testes (STBM) and injected with complete Freund's adjuvant into Wistar rats. In 60% of animals a mild multifocal orchitis was observed. In damaged areas, perivascular and peritubular mononuclear cell infiltrates and different degrees of cell sloughing of some seminiferous tubules were observed.

The role of interleukin 1 in acute phase serum amyloid A (SAA) and serum amyloid P (SAP) biosynthesis.

The acute phase SAA and SAP profiles have been compared for localized and endotoxin induced inflammation in LPS responder and nonresponder strains of mice. The SAP profile can reflect a delay with respect to the start of the increase. Its maximum is on the order of ten times the nonacute phase concentration and elevated concentrations are sustained 24 to 48 hours after SAA concentration is rapidly decreasing to normal.

Mechanism of immune transfer by RNA extracts. Immune RNA induces the synthesis of idiotype-bearing antigen receptors in noncommitted cells.

Immune RNA (I-RNA) was extracted form lymphoid organs of BALB/c mice immunized with AKR lymphoid cells. Incubation of normal BALB/c spleen cells with this I-RNA (but not with normal RNA) resulted in leukocyte migration inhibition reactions (LMIR) against AKR extracts but not against purified protein derivative or BALB/c sarcoma extracts. This transfer was abolished by pretreating I-RNA with RNAse but not with pronase.

Transfer of cell migration inhibition in vitro with xenogeneic RNA in experimental allergic orchitis.

Experimental allergic orchitis (EAO) was induced in rats following the injection of homologous testicular homogenate (THr) emulsified in Freund's complete adjuvant. Immune RNA (iRNA) was extracted from the spleen and lymph nodes. Normal guinea-pig peritoneal exudate cells (GP-PEC), when incubated in vitro with iRNA, were able to specifically recognise and respond to the immunising antigens (THr and PPD) as assessed by the direct migration inhibition reaction (MIR).

In vitro transfer of cellular immunity in experimental allergic orchitis by means of immune RNA.

Ribonucleic acid (RNA) extracts were obtained from lymph nodes of guinea-pigs that had previously been immunized with a purified testicular antigen emulsified in Freund's complete adjuvant. The RNA extracts were incubated with normal guinea-pig peritoneal exudate cells (NGP-PEC). After treatment, the NGP-PEC cells showed specific inhibition of migration when tested with the specific antigen.

Idiotypic determinants in alloantigen receptors. I. Role in a leucocyte migration inhibition reaction.

An anti-idiotypic serum was prepared by injecting BALB anti-AKR serum into (BALB X AKR)F1 mice. Pretreatment of BALB anti-AKR immune cells with this anti-idiotypic serum plus complement abrogated a leucocyte migration inhibition reaction (LMIR) against AKR extracts but not against purified protein derivative By itself, the serum induced LMIR in immune cells but not in normal cells. The reaction was strain-specific and anti-Thy 1,2 plus complement sensitive.

Transfer of experimental allergic orchitis with immune RNA studies in vivo.

Ribonucleic acid extracts (RNA) obtained from the lymph nodes and spleens of guinea pigs, which were immunized with testicular antigen emulsified in Freund's complete adjuvant (FCA), were injected intraperitoneally into normal guinea pigs. The transferred guinea pigs developed a delayed hypersensitivity to sperm antigens and testicular lesions which resembled the lesions obtained in the donor RNA guinea pigs. When the transfer was performed with RNA extracted from guinea pigs immunized with FCA alone or with 'immune' RNA treated with Ribonuclease, neither cellular immunity nor testicular lesions were observed.