Leukocyte Adherence Inhibition Reactivity Research Articles

Tumor size, leukocyte adherence inhibition and serum levels of tumor antigen in dogs with the canine transmissible venereal sarcoma.

Tumor antigen (TA) associated with the canine transmissible venereal sarcoma (CTVS) was detected in the sera of dogs bearing the tumor. Rabbit antisera specific for tumor antigen and 3 M KCl extracts of CTVS cells were used in both a competitive enzyme-linked immunosorbent assay (ELISA) and antigen-capture ELISA to quantify levels of circulating TA. In a study of 29 dogs bearing the transplanted CTVS, levels of circulating TA correlated positively with tumor volume. In a longitudinal study of four dogs receiving a transplant of 10(8) viable CTVS cells, circulating CTVS antigen was detected transiently 2 days after transplantation, while persistent levels of TA associated with increasing tumor volume were demonstrable 19-34 days after transplantation. In three of four tumor-bearing dogs, levels of serum TA correlated inversely with values obtained with peripheral blood leukocytes in the leukocyte adherence inhibition (LAI) assay; elevated levels of circulating TA found in dogs with large (greater than 7 cm3) tumors were associated with decreased LAI reactivity of peripheral blood leukocytes. TA could not be detected in sera 48-72 h after surgical removal of CTVS whereas LAI reactivity of peripheral blood leukocytes to CTVS antigen rebounded 1-3 weeks following tumor excision. Results of this study support the use of the competitive ELISA and LAI techniques in assessing levels of circulating tumor antigen, tumor burden and tumor-specific immunity.

Effect of aggregated IgG on mononuclear and polymorphonuclear cell cooperation.

The leukocyte adherence inhibition (LAI) test was used to determine the response of different leukocyte subpopulations in rheumatoid arthritis (RA) patients and normal donors to heat-aggregated gammaglobulins (HAGGs). The adherence of polymorphonuclear cells of (PMNs) could be inhibited either directly by high concentrations of HAGGs or indirectly by soluble factors secreted by RA mononuclear cells incubated with low amounts of HAGGs. The stimulatory site of the IgG was located on the Fc fragment. Since the LAI reaction was also observed with material recovered from rheumatoid synovial fluid, tissue, and nodules, these results could have clinical relevance in RA.

Cell-populations involved in the humoral leukocyte adherence inhibition reaction. The T8-suppressor/cytotoxic cells are both effectors and responders

In an attempt to identify the cell subpopulation involved in the humoral leukocyte adherence inhibition (H-LAI) reaction, mononuclear leukocytes were fractionated and the response with the different cell populations was measured in the H-LAI assay using sera from lung cancer patients and a lung cancer associated antigen. The monocytes were found to exhibit a suppressive effect on the H-LAI response. The B-lymphocytes seemed not to take an active part in the reaction. Depletion of the T-lymphocytes abolished the reaction. Subsequent studies on the T-lymphocyte subpopulations revealed that removal of the T 4-cells had little effect while removal of the T 8-cells resulted in complete abrogation of the H-LAI response. Direct blocking by monoclonal antibodies against the T 4 and T 8 surface determinants gave additional support for the T 8-cell dependency of the H-LAI assay. The cells that specifically were induced to loose adherence in the H-LAI assay upon incubation with serum from a lung cancer patient and lung cancer associated antigen were also analyzed. Compared to the total mononuclear leukocyte population, the relative content of monocytes and B-cells were lower in the non-adherent population. An increase was found in the relative number of T-cells. While the relative number of T 4-cells decreased, the content of T 8-cells was significantly increased. Furthermore, a direct correlation was found between the loss of adherence of the T 8-subpopulation and the index of the H-LAI response. The present study indicates the T 8-subpopulation of the T-lymphocytes to be involved both in the effector and responder side of the H-LAI reaction and gives implications for an immunological reaction behind the response of the H-LAI assay.

Leukocyte adherence inhibition in patients with nonmalignant disorders of the colon and colorectal cancer.

The tube leukocyte adherence inhibition (LAI) technique was used to investigate the antitumor immunity in two groups of patients generally considered to be at "high risk" of developing colorectal cancer. The first group comprised 21 patients with colorectal polyps and the second 12 patients with various forms of colitis. Also 29 patients with histologically confirmed colorectal cancer were tested. The tube LAI assay was performed using peripheral blood leukocytes from individual patients and crude extracts of colorectal and breast cancers. Positive LAI reactions were observed in 18 out of 29 (62%) patients with colorectal cancer, in 1 out of 21 (5%) patients with colorectal polyps and in 1 out of 12 (8%) patients with colitis. The results indicate that in confirmed cases of malignancies, sensitization to colon tumor-associated antigens could be detected in the tube LAI test, whereas, premalignant sensitization to these antigens in "high risk" groups of patients could not be demonstrated.

New micro-glass-tube leukocyte adherence inhibition assay assessing cell adherence of mononuclear cell subpopulations defined by monoclonal antibodies

A new micro-glass-tube leukocyte adherence inhibition (LAI) assay which is appropriate for detecting delayed type hypersensitivity in vitro has been developed for human leukocytes. Enumeration of adherent cells is replaced by a cellular radioimmunoassay determining antibody binding of the monoclonal reagents, OKT4, OKT8, and OKM1, to glass-adherent cells, fixed by glutaraldehyde or formaldehyde. An LAI reactivity to purified protein derivative of tuberculin (PPD) was detectable in donors giving a positive PPD skin test with OKT4 reagent, but not with the other two reagents.

Mechanism of the LAI Test in Bladder Cancer Patients

To clarify the mechanism of the leukocyte adherence inhibition (LAI) test, 30 bladder cancer patients were studied by the fractionated LAI test in which peripheral lymphocytes were separated into monocyte rich and monocyte deplete fractions. The mean LAI reactivity of 30 bladder cancer patients on the monocyte rich fraction (43.2 ± 20.3 per cent) was significantly higher than that of the corresponding patients on the standard LAI test (30.4 ± 12.7 per cent), whereas the mean LAI reactivity of these patients on the monocyte deplete fraction (15.6 ± 10.7%) was significantly lower than that on the standard LAI test of the same patients (respectively p <0.001 and p <0.01). It suggests that monocytes play an important role in the capillary LAI test.To further comprehend the mechanism of the LAI phenomenon, indicator cells involved in the LAI test were observed by transmission and scanning electron microscopy. The microvilli on the cell surface of nonadherent monocytes of bladder cancer patients were decreased in number and shortened in length but other populations of nonadherent cells were not remarkably changed. These observations showed that the bladder tumor antigens in extracts from tumors appear to have an influence on the microvilli of monocytes, specifically on monocytes from bladder cancer patients. These morphological changes correlate with the results from fractionated LAI assay and may result in the tumor antigen specific LAI reactivity observed in leukocytes of bladder cancer patients.

Leukocyte adherence inhibition (LAI) in rats bearing transplantable syngeneic tumors of different immunogenicity

The tube leukocyte adherence inhibition (LAI) assay was used to follow the LAI response in inbred BN rats with subcutaneously (s.c.) transplanted syngeneic liposarcoma (LS 175) tumor and in inbred WAG rats with s.c. transplanted syngeneic colon (CC 531) and skin ( 1618) tumors. Initially, the tube LAI assay was used to follow the LAI reactivity of peripheral blood leukocytes (PBL) from BN rats bearing tumor LS 175. Sporadic LAI reactivity was observed in the PBL of these rats when incubated with a specific crude tumor extract for either 2 or 20 hr. No definite conclusion regarding the lack of significant tumor-specific LAI reactivity could be drawn since LS 175 is a non-immunogenic tumor. Therefore additional LAI studies were performed with the weakly immunogenic tumor CC 531 and the highly immunogenic tumor 1618 in WAG rats. Surprisingly, only sporadic LAI reactivity was observed in the PBL of rats bearing either the CC 531 or the 1618 tumors using both the 2 and 20 hr LAI assays. This absence of tumor-specific LAI reactivity was particularly remarkable in the highly immunogenic 1618 tumor-bearing rats, since it would suggest that the antigen(s) responsible for its high immunogenicity could not evoke any consistent LAI reactivity. Since oxidative metabolites of arachidonic acid have been shown to be the final mediators of chemoattractant-induced LAI, the adherence inhibition effect of leukotriene B 4 (LTB 4) on the PBL of BN and WAG rats was also investigated in order to exclude the possibility that the lack of consistent LAI reactivity was due to a lack of responsive cell population in the PBL. PBL of both BN and WAG rats showed a significant increase in the adherence inhibition in the presence of LTB4, suggesting that the sporadic LAI reactivity was not due to a lack of responsive cell population.

Leukocyte Adherence Inhibition to Myelin Basic Protein by Cancer Patients' T-Lymphocytes in Association With Class II Major Histocompatibility Antigens on Monocytes&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;

Patients' leukocytes were shown to react consistently in tube leukocyte adherence inhibition (LAI) assays with myelin basic protein (MBP) at optimal concentration, whereas control leukocytes were nonreactive. Mononuclear cells from patients with cancer gave positive LAI reactions with MBP, but separated T-lymphocytes, monocytes, and neutrophils did not. The mononuclear cell LAI responses were blocked by monoclonal antibody (MAb) to monomorphic determinant of class II major histocompatibility complex (MHC) antigens and to T4+ (Leu-3a+) and T3+ (Leu-4+) T-cell differentiation antigens but not by antibody to class I MHC antigens or T8+ (Leu-2a+) antigens. MBP was thus recognized by helper T-cells, requiring presentation in association with class II MHC determinants on monocytes. MAb to class I and class II MHC antigens and to T8+ (Leu-2a+), T4+ (Leu-3a+), and T3+ (Leu-4+) differentiation antigens did not negate LAI mediated by peripheral blood lymphocytes to organ-specific cancer neoantigens (OSN) of crude extracts of allogeneic cancer, which had previously been shown to react with cytophilic antibody on allogeneic monocytes. When membrane OSN and leukocytes were autologous, T8+ (Leu-2a+) phenotypic T-cells also mediated LAI that was blocked by anti-T8 (Leu-2a) and anti-T3 (Leu-4). LAI induced by MBP was also negated by drugs that antagonize thromboxane-leukotriene biosynthesis, indicating that, in common with other LAI reactions, the terminal mediators of nonadherence are oxidative metabolites of arachidonic acid. In addition to clarifying the role of MBP in the cellular in vitro immunoreactivity of cancer patients, the present observations have important implications for theories of LAI. Sensitized leukocytes have different mechanisms for the recognition of antigens in different forms, and the antigen-stimulated leukocytes produce mediators that in a final common pathway induce nonadherence of surrounding cells through leukotriene-like metabolites.

Monoclonal antiidiotypic antibodies related to a murine oncofetal bladder tumor antigen induce specific cell-mediated tumor immunity.

Rat monoclonal antibody 6.10 recognizes a 175-kDa protein expressed in all BALB/c mouse transitional cell bladder carcinomas tested, in epithelial cells of the mouse embryo, and in a few epithelial cells of adult mice. The antibody was used as an immunogen to generate two mouse monoclonal antibodies, 21D9 and 43A10, which bind to idiotopes on antibody 6.10 associated with the binding site for the 175-kDa antigen. The antiidiotypic antibodies induced bladder tumor-specific, cell-mediated immunity when injected into syngeneic mice, as shown by delayed-type hypersensitivity reactions in vivo and leukocyte adherence inhibition reactions in vitro. Tumor specificity was demonstrated by employing as controls a chemically induced BALB/c fibrosarcoma, MCA-1511 (MCA, 3-methylcholanthrene), and its corresponding antiidiotypic antibody, 5.96. Lymphocytes from mice sensitized with antibody 21D9 or 5.96 specifically recognized antigens in extracts of BALB/c bladder carcinoma BTCC-1660 (BTCC, bladder transitional cell carcinoma) and sarcoma MCA-1511, respectively, as shown by leukocyte adherence inhibition reactivity. This reactivity was selectively abrogated by prior treatment of the sensitized cells with the appropriate antiidiotypic antibodies and complement. An antigen recognized in vitro by antibody 21D9-sensitized lymphocytes could be separated from BTCC-1660 extract by immunoabsorption with antibody 6.10 and elution with acidic buffer. Our findings indicate that the oncofetal antigen defined by antibody 6.10 is recognized by the immune system of syngeneic mice and suggest that antiidiotypic antibodies related to certain oncofetal antigens can be used to immunize against syngeneic tumors.

Evaluation of leukocyte adherence inhibition (LAI) test in primary and secondary hepatic malignancies.

Leukocyte adherence inhibition (LAI) has been demonstrated to be a simple, rapid, and reliable technique in the diagnosis of various malignancies including hepatocellular carcinoma. The LAI test was carried out employing modified tube LAI technique in patients with primary hepatocellular carcinoma (HCC) and secondary carcinomas of liver. Positive LAI response to HCC antigen was obtained in all six (100%) cases of hepatocellular carcinoma tested. None of the control cases, which included 8 healthy subjects and 16 cases of benign liver diseases, gave positive LAI response. Two out of 19 cases of secondary carcinoma gave a positive LAI reaction to HCC antigen. In secondary carcinomas, 19 out of 21 cases (90.48%) gave positive LAI reaction to secondary adenocarcinoma antigen. There were two false positives in controls (1 each of cirrhosis and amebic liver abscess), and 1 out of 8 cases of HCC also gave positive response to secondary carcinoma antigen. Thus, LAI test was found to be useful in the diagnosis of hepatic malignancies.

Amplification of lymph node cell tube leukocyte adherence inhibition (LAI) reactivity by leukocyte adherence inhibition factor (LAIF)

This investigation examines the immunologic basis for specific antigen-induced tube leukocyte adherence inhibition (LAI) reactivity of draining lymph node cells (LNC) from dogs with canine transmissible venereal sarcoma (CTVS). CTVS regresser LNC, macrophage-depleted LNC, and enriched T lymphocyte fractions, but not enriched B lymphocyte fractions, were specifically reactive to CTVS antigen extract in direct tube LAI. In addition, regressor LNC amplified tube LAI responses by generating supernatants with leukocyte adherence inhibition factor (LAIF) activity for normal dog indicator LNC and enriched peripheral blood mononuclear cells (PBMC) in an indirect tube LAI assay. However, macrophage-depleted LNC and enriched T lymphocyte fractions failed to generate supernatants with LAIF activity, suggesting that macrophage accessory cells play a central role in the amplification of tube LAI. Interestingly, CTVS regressor peripheral blood leukocytes (PBL) and PBMC, which were specifically reactive in direct tube LAI, also failed to generate supernatants with LAIF activity. These findings demonstrate a distinction between LAIF-mediated amplification and direct tube LAI reactivity, and suggest that leukocyte populations with differing cellular proportions and from different immunologic compartments may participate in tube LAI via different mechanisms.

A two-chain tumour-related suppressor factor specific for a sequence antigen

Suppressor factors in the serum of CBA mice bearing transplanted methylcholanthrene-induced tumours suppressed the leukocyte adherence inhibition reaction between tumour-sensitized peritoneal cells and a sequenced antigen, myelin basic protein (MBP). Chromatography on Sephacryl S-200 columns demonstrated suppressive activity in low molecular weight fractions (40–50 kDa) derived from whole serum. The factors were absorbed from serum by MBP, but not by lysozyme, coupled to Sepharose gel. Cleavage with sodium dodecyl sulphate (SDS) and absorption with either MBP or anti-I-J antibody on Sepharose gels yielded inactive supernatants that regained suppressive activity when combined. Elution of these gels with acidic buffer yielded eluates that were inactive alone but suppressive when combined. These results indicate that the tumour-related suppressor factors consist of two chains separable by detergent action; one chain is antigen (MBP)-binding and the other contains an I-J determinant.

Detection of different states of immunity to colon cancer in rats by a leukocyte adherence inhibition (LAI) assay assessing the adherence of T lymphocytes and monocytes selectively.

Peripheral blood mononuclear cells (MNC) of rats, which had received a subcutaneous inoculation of either viable or X-irradiated syngeneic DMH-W49 colon carcinoma cells, were investigated sequentially for sensitization against tumor-associated antigens by a new micro-glass-tube leukocyte adherence inhibition (LAI) assay. The number of adherent cells of MNC subpopulations was estimated by a cellular radioimmunoassay (CRIA), which utilizes anti-monocyte (MC) antiserum or anti-T-cell monoclonal antibody (McAb) and 125I-labelled protein A. LAI reactivity was demonstrated in rats sensitized with X-irradiated tumor cells when assessing the adherence of both T lymphocytes and monocytes. It was found that reactivity with the two different types of indicator cells did not usually coincide in time. The same phenomenon was also observed in tumor-bearing rats although with lower levels of LAI reactivity. In both groups the LAI response detected by anti-T-cell reagent mostly appeared earlier after tumor-cell inoculation than the response demonstrated by anti-MC serum. The T-lymphocyte-associated reactivity also disappeared more rapidly. These results suggest that different states of immune reactivity are reflected in LAI responses involving T lymphocytes and monocytes as indicator cells.

Immunity to Tumor-Associated Antigens in Vasectomized Men

Leukocytes from 49 vasectomized and 57 age-matched nonvasectomized men were tested in the leukocyte adherence inhibition (LAI) assay for reactivity to sperm and various 3-M KCl human tumor extracts. Forty-four percent of the vasectomized men and 15% of the control group were reactive to the sperm antigen preparation (P less than or equal to 0.03). Similarly, a significantly higher percentage of vasectomized men responded to 3 of 5 tumor extracts tested: melanoma I (34.7 vs. 15.8%, P less than or equal to 0.04), squamous cell carcinoma (48.8 vs. 26.0%, P less than or equal to 0.04), and breast carcinoma (19.5 vs. 4%, P less than or equal to 0.04). Thirty percent of vasectomized versus 4% of the control group responded to more than two tumor antigens (P less than or equal to 0.03). The degree of LAI reactivity to each tumor extract was highly correlated with degree of antisperm LAI reactivity, and the degree of LAI responsiveness to one of the melanoma extracts was significantly correlated with antisperm antibody titer as measured by the sperm-immobilization assay. Furthermore, nonresponsive leukocytes from the control population converted to tumor antigen-responsive when incubated with sera from vasectomized LaI-positive men. Data from this study indicated that a large percentage of vasectomized men with sperm immunity were responsive to tumor-associated antigens in the LAI test and that antisperm antibodies or other serum factors played a role in this response. These results and the evidence that most tumor antigen-responsive cancer patients also have serum antibodies that reacted with sperm suggested that vasectomized men and cancer patients frequently responded to immunologically cross-reactive antigenic determinants present on both sperm and tumor cells.

Cellular origin of blocking factors from cultured spleen cells of tumor-bearing mice

Spleen cells from mice bearing methylcholanthrene-induced tumors were cultured for 2 days without further stimulation. Blocking factors were consistently detected in culture supernatants by their ability to suppress leukocyte adherence inhibition reactions between soluble tumor antigens and peritoneal cells of tumor-bearing mice. The blocking factors were specific for individual tumors. The cellular origin of these factors was investigated by depleting the spleen cell population of various cell types before culturing. The cells involved were removed by treatment with antibodies to certain membrane markers (Thy-1, Ly-2, Ia, I-J) but not by anti-Ly-1 antibodies. Removal of adherent cells also prevented production of blocking factors, which was restored by reconstitution with syngeneic but not allogeneic cells from normal mice. The normal reconstituting cells were shown to bear Ia, but not I-J or IgM. This indicates that blocking factors (previously shown to have I-J determinants in their molecules) originate from suppressor T lymphocytes (Thy-1 +, Ly-1 −2 +, I-J +), with macrophages (I-J −, Ia +) in the role of accessory cells.

The early detection of host immune response to spontaneous mouse mammary tumors by leukocyte adherence inhibition

Longitudinal testing of C3H/HeJ female mice was carried out over a 52-week period with the leukocyte adherence inhibition (LAI) assay using solubilized tumor antigen prepared by 3 M KCl extraction. During this period, 75% of the mice developed histologically confirmed mammary adenocarcinomas. Of those mice 93% had a statistically significant P < 0.01) LAI response to soluble mammary tumor antigen prior to first detection of tumors by palpation. Five percent of the test group developed statistically significant LAI responses without development of detectable mammary tumors within a 34-week observation period. The first significant LAI reactivity of individual mice preceded the first detection of tumors by an average of more than 17 weeks.

Regulation of Cell-Mediated Immunologic Reactivity to Moloney Murine Sarcoma Virus-Induced Tumors. III. Further Characterization of Tumor-Specific Serum Blocking Factors&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;

Blocking factors in the sera of inbred CBA mice bearing either Moloney murine sarcoma virus-induced tumors or transplanted 3-methylcholanthrene-induced tumors specifically blocked in the leukocyte adherence inhibition reaction between tumor-sensitized peritoneal cells and tumor antigens. These factors were absorbed from serum by treatment with anti-Ia antibodies and could be eluted in a partially purified form. Chromatography on Sephacryl S-200 columns demonstrated blocking activity in fractions of high and low molecular weight (greater than 100,000 and 40,000--50,000, respectively) derived from whole sera or eluates. Active fractions from serum appeared to retain the tumor specificity of the original material.

Immunity to Tumor-Associated Antigens in Vasectomized Men&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn3"&gt;3&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn4"&gt;4&lt;/xref&gt;

Leukocytes from 49 vasectomized and 57 age-matched nonvasectomized men were tested in the leukocyte adherence inhibition (LAI) assay for reactivity to sperm and various 3-M KCl human tumor extracts. Forty-four percent of the vasectomized men and 15% of the control group were reactive to the sperm antigen preparation (P less than or equal to 0.03). Similarly, a significantly higher percentage of vasectomized men responded to 3 of 5 tumor extracts tested: melanoma I (34.7 vs. 15.8%, P less than or equal to 0.04), squamous cell carcinoma (48.8 vs. 26.0%, P less than or equal to 0.04), and breast carcinoma (19.5 vs. 4%, P less than or equal to 0.04). Thirty percent of vasectomized versus 4% of the control group responded to more than two tumor antigens (P less than or equal to 0.03). The degree of LAI reactivity to each tumor extract was highly correlated with degree of antisperm LAI reactivity, and the degree of LAI responsiveness to one of the melanoma extracts was significantly correlated with antisperm antibody titer as measured by the sperm-immobilization assay. Furthermore, nonresponsive leukocytes from the control population converted to tumor antigen-responsive when incubated with sera from vasectomized LaI-positive men. Data from this study indicated that a large percentage of vasectomized men with sperm immunity were responsive to tumor-associated antigens in the LAI test and that antisperm antibodies or other serum factors played a role in this response. These results and the evidence that most tumor antigen-responsive cancer patients also have serum antibodies that reacted with sperm suggested that vasectomized men and cancer patients frequently responded to immunologically cross-reactive antigenic determinants present on both sperm and tumor cells.

T&lt;sub&gt;G&lt;/sub&gt; Cell Involvement in the Leukocyte Adherence Inhibition Phenomenon&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn3"&gt;3&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn4"&gt;4&lt;/xref&gt;

Peripheral blood mononuclear cells (PBMC), T-cells, non-T-cells, TG cells, and TM cells were tested for leukocyte adherence inhibition (LAI) reactivity to purified protein derivative (PPD) in normal human volunteers to determine the reactive cell subfractions. T-cells were separated by sheep red blood cell rosetting and TM and TG cells by rosetting with anti-ox red blood cell (ORBC) IgM- and IgG-treated ORBC. Fresh PBMC, T-cells, and TG cells gave positive LAI reactivity to PPD in PPD-positive donors only. PBMC that had undergone 24-hour incubation or extensive washing, non-T-cells, and TM cells were unreactive. All cell subfractions were negative in PPD-negative donors. Indirect LAI assay was performed on the spent media from overnight incubation of unstimulated PBMC and also following a 1-hour incubation of the various cell subfractions obtained from a PPD-reactive donor with PPD. Positive reactions, indicating the release of an LAI factor (LAIF), were obtained with the spent media and with the T-cell and TG cell subfractions following PPD stimulation, whereas non-T-cell and TM cell subfractions yielded no reactivity. Incubation of sensitized T-cells with PPD in the presence of cycloheximide and preincubation of T-cells for 24 hours with cycloheximide before PPD exposure failed to inhibit LAI reactivity. These data suggest that T-cells, specifically TG cells, can release LAIF upon specific antigen stimulation with PPD, whereas non-T-cell and TM cell subpopulations fail to respond to the same stimulus. LAIF may also be released into the culture media with prolonged (overnight) incubation in artificial media or with extensive washing. Inhibition of protein synthesis during antigen exposure or up to 24 hours before antigen exposure does not appear to inhibit LAI reactivity.

Leukocyte adherence inhibition test in renal diseases.

Leukocyte adherence inhibition (LAI) test was examined in 35 patients with renal diseases and 14 normal controls, using collagenase-treated glomerular basement membrane, glycosidase-treated glomerular basement membrane and renal tubular epithelium as antigens. Although the control group showed strikingly similar mean LAI indices for all antigens tested, the whole group of patients with renal diseases showed a wide scatter of values. Two categories of patients had significantly increased LAI indices (p less than 0.01) when their mean values were compared with those of normal controls: (1) rapidly progressive glomerulonephritis (RPGN) and (2) lupus nephritis (SLE). In the serial studies of the RPGN and SLE cases, there were no significant changes in the pattern of LAI and they continued to give positive and very comparable results when re-examined at intervals of 1-6 months. Out of the 30 patients who were able to be evaluated with the three antigens, 15 cases exhibited positive LAI response to two or more antigens simultaneously. These in vitro findings suggest that there is an abnormal cellular response to certain antigen or widespread LAI reactivity to a variety of renal antigens in certain forms of human glomerulonephritis.