Lichen planus (LP) is a common oral disorder which may represent the manifestation of a mucosal reaction to a variety of aetiological factors. Of the many immunological changes described in LP several may be epiphenomena although a cell-mediated immune response to unidentified antigens or antigenic changes clearly is involved. Associations with drugs or systemic disorders are well-defined in some patients but may, in others, be aleatoric. Finally, the prognosis of oral LP not only differs from that of cutaneous LP but there is little doubt that in a few instances LP is a premalignant condition.

Lichen planus. review and update on pathogenesis

Studies on oral lichen planus. II. Follow-up on 200 patients, clinical characteristics, and associated malignancy.

Deposits of immunoglobulins, complement, and fibrinogen in oral lupus erythematosus, lichen planus, and leukoplakia

Objective: Oral lichen planus (OLP) presents with various clinical forms that can be classified into 2 major types: reticular OLP and atrophic-erosive OLP. Our objective was to investigate immunologic differences between these 2 types. Study Design: We investigated possible immunologic differences between 26 patients with reticular OLP and 26 patients with atrophic-erosive OLP. Results: No differences were detected in serum Ig levels or complement levels. However, the mean proportions of CD4+CD45RO+ and DR+ lymphocytes were significantly higher in patients with atrophic-erosive OLP than in patients with reticular OLP, whereas the mean proportion of CD8+CD45RA+ lymphocytes was significantly lower in patients with atrophic-erosive OLP. Conclusion: These findings suggest that the 2 clinical types of OLP might have different immunopathogenic mechanisms. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;91:180-8)

Peripheral T-cell subsets in patients with reticular and atrophic-erosive oral lichen planus.

Histochemical identification of T cells in oral lichen planus

In this preliminary study we explored the possibility of an immunologic component in oral lichen planus by assessment of serum immunoglobulins and complement levels, by skin tests for cellular immunity, and by fluorescent antibody techniques to detect immunoglobulins in the lesions. Although certain abnormalities were noted, none was consistent or of significant magnitude to clarify the cause of this disease.

Studies on Oral Lichen Planus : I. Serum Immunoglobulins and Complement

Background In preclinical studies of pancreatic ductal adenocarcinoma (PDAC), ibrutinib improved the antitumor efficacy of the standard of care chemotherapy. This led to a phase 1b clinical trial to determine the safety, tolerability, and immunologic effects of ibrutinib treatment in patients with advanced PDAC. Methods Previously untreated patients with PDAC were enrolled in a phase 1b clinical trial (ClinicalTrials.gov) to determine the safety, toxicity, and maximal tolerated dose of ibrutinib when administered with the standard regimen of gemcitabine and nab-paclitaxel. To study the immune response to ibrutinib alone, the trial included an immune response arm where patients were administered with ibrutinib daily for a week followed by ibrutinib combined with gemcitabine and nab-paclitaxel. Endoscopic ultrasonography-guided primary PDAC tumor biopsies and blood were collected before and after ibrutinib monotherapy. Changes in abundance and functional state of immune cells in the blood was evaluated by mass cytometry by time of flight and statistical scaffold analysis, while that in the local tumor microenvironment (TME) were assessed by multiplex immunohistochemistry. Changes in B-cell receptor and T-cell receptor repertoire were assessed by sequencing and analysis of clonality. Results In the blood, ibrutinib monotherapy significantly increased the frequencies of activated inducible T cell costimulator+(ICOS+) CD4+ T cells and monocytes. Within the TME, ibrutinib monotherapy led to a trend in decreased B-cell abundance but increased interleukin-10+ B-cell frequency. Monotherapy also led to a trend in increased mature CD208+dendritic cell density, increased late effector (programmed cell death protein 1 (PD-1–) eomesodermin (EOMES+)) CD8+ T-cell frequency, with a concomitantly decreased dysfunctional (PD-1+ EOMES+) CD8+ T-cell frequency. When ibrutinib was combined with chemotherapy, most of these immune changes were not observed. Patients with partial clinical responses had more diverse T and B cell receptor repertoires prior to therapy initiation. Conclusion Ibrutinib monotherapy skewed the immune landscape both in the circulation and TME towards activated T cells, monocytes and DCs. These effects were not observed when combining ibrutinib with standard of care chemotherapy. Future studies may focus on other therapeutic combinations that augment the immunomodulatory effects of ibrutinib in solid tumors. Trial registration number NCT02562898.

/pdf/modulation-of-myeloid-and-t-cells-in-vivo-by-brutons-19g96z1f.pdf

Modulation of myeloid and T cells in vivo by Bruton’s tyrosine kinase inhibitor ibrutinib in patients with metastatic pancreatic ductal adenocarcinoma

Abstract No. 266 Phase I Prospective Trial of TAS-102 (Trifluridine and Tipiracil) and Radioembolization with 90Y Resin Microspheres for Chemo-Refractory Colorectal Liver Metastases

110 Background: Clinical efficacy of Yttrium-90 (90Y) radioembolization (TARE) for patients with chemotherapy-refractory metastatic colorectal cancer (mCRC) is limited by extrahepatic disease progression. TAS-102 (trifluride and tipiracil) has overall survival benefit for patients with refractory mCRC and may be a radiosensitizer. We aimed to evaluate the safety of the combination of TAS-102 and 90Y resin TARE in a Phase I dose-escalation trial. Methods: Adult patients with bilobar liver-dominant chemo-refractory mCRC were treated with sequential Y90 resin TARE (body surface area dosimetry) in combination with TAS-102 (20mg/m2, 27mg/m2, and 35mg/m2) in 28-day cycles according to 3+3 dose-escalation design. Beginning with cycle 3, TAS-102 was administered as monotherapy until disease progression or development of intolerable toxicity. Primary objectives were to determine maximum tolerated dose (MTD) of TAS-102, to assess toxicity, and to establish safety of TAS-102 in combination with 90Y TARE. Results: A total of 14 patients (10 women, 4 men) have been treated to date. Among 9 patients enrolled in the dose-escalation phase, no dose limiting toxicities were observed. The MTD of TAS-102 in combination with Y90 was 35mg/m2, which was selected for the dose expansion phase. Severe adverse events (AEs) included: neutropenia (46%); anemia (23%); and thrombocytopenia (8%), which were attributed to TAS-102. All other AEs were mild and transient. At least one follow-up imaging study has been obtained for 13 patients, and 10 patients have completed trial participation. Disease control rate in the liver was 100%. Conclusions: The combination of TAS-102 and 90Y TARE for patients with liver-dominant mCRC is safe and consistently achieved disease control within the liver. Severity and incidence of AEs is within the expected range of TAS-102 and 90Y TARE monotherapy. A dose-expansion phase with planned enrollment of 12 patients is ongoing. Clinical trial information: NCT02602327.

Phase I prospective trial of TAS-102 (trifluride and tipiracil) and radioembolization with 90Y resin microspheres for chemo-refractory colorectal liver metastases.

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Studies on Oral Lichen Planus : I. Serum Immunoglobulins and Complement

Modulation of myeloid and T cells in vivo by Bruton’s tyrosine kinase inhibitor ibrutinib in patients with metastatic pancreatic ductal adenocarcinoma

Abstract No. 266 Phase I Prospective Trial of TAS-102 (Trifluridine and Tipiracil) and Radioembolization with 90Y Resin Microspheres for Chemo-Refractory Colorectal Liver Metastases

Phase I prospective trial of TAS-102 (trifluride and tipiracil) and radioembolization with 90Y resin microspheres for chemo-refractory colorectal liver metastases.