Protection of Quiescence and Longevity of IgG Memory B Cells by Mitochondrial Autophagy

Kodali, Srikanth; Li, Min; Budai, Marietta Margit; Chen, Min; Wang, Jin

doi:10.4049/jimmunol.2100969

Cited by 9 publications

(7 citation statements)

References 93 publications

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“…B220 + CD3 -CD27 + memory B cells were also assessed in our study. These antigenspecific memory cells were first described over 20 years ago and are responsible for quick response upon antigen restimulation by switching to a B220 low phenotype [74,75]. This may indicate that EXP-2.3 was sensitized to OVA during the CD, which has been observed in previous studies in our group [32] and also in the literature [76,77].…”

Section: Discussionsupporting

confidence: 79%

Expansion of Antigen- Specific Memory Cells as a Potential Booster for Food Tolerance Induction

Silva¹,

Marmello²,

Bentes³

et al. 2023

Preprint

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Approximately 3% of children in Western countries are diagnosed with peanut allergy, a likely lifelong disease. The preferred treatment for food allergy is allergen avoidance. However, oral immunotherapy is an FDA-approved treatment to re-induce tolerance, still, not all patients respond as expected. Thus, the aim of this work is to evaluate whether the association of an antigen-specific tolerogenic (oral tolerance) bystander effect can ameliorate the recovery of inflamed intestinal mucosa. Adult male C57BL/6 mice were divided into five groups, four of which were submitted to an intestinal inflammation induction protocol to peanuts. After sensitization, experimental groups were orally challenged with either peanuts or a hybrid diet (peanuts + mouse chow). In a second stage, groups were sensitized, challenged with peanuts, and then received either peanuts, hybrid diet, or ovalbumin chow during the recovery period of the inflamed mucosa. Results showed no changes in diet intake and body weight. Polyisotypic anti-peanut IgG and IgG1 were significantly increased in the serum from animals in allergic groups. The group that received the hybrid diet showed an increase in CD4+CD25+Foxp3+ regulatory T cells, as well as in B220+CD3-CD27+ memory B cells. Histology of the duodenum showed a decrease in intraepithelial leukocytes in animals who received hybrid diet. Together, our results show that when the tolerogen is added to a diet containing the allergen, it can ameliorate the induction of local inflammation. Simultaneously offering the allergen with a tolerated food increased the mucosal recovery due to the expansion of previously induced memory cells.

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Section: Discussionsupporting

confidence: 79%

Expansion of Antigen- Specific Memory Cells as a Potential Booster for Food Tolerance Induction

Silva¹,

Marmello²,

Bentes³

et al. 2023

Preprint

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“…Mice lacking mitochondrial autophagy genes accumulate mitochondria and experience oxidative phosphorylation and fatty acid synthesis, leading to the loss of B memory cells. 188 Similarly, autophagy facilitates the differentiation of monocytes to macrophages stimulated by colony-stimulating factor 1 (CSF1) and CSF2. Mechanically, CSF1 promotes autophagy by increasing the expression and phosphorylation of ULK1.…”

Section: Autophagy Synergizes Antitumor Immune Responsementioning

confidence: 99%

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Gao

Wang

Zhou

et al. 2022

Sig Transduct Target Ther

316

189

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In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly limits the application of ICIs. Converting these immune “cold” tumors into “hot” tumors that may respond to ICIs is an unsolved question in cancer immunotherapy. Since it is a general characteristic of cancers to resist apoptosis, induction of non-apoptotic regulated cell death (RCD) is emerging as a new cancer treatment strategy. Recently, several studies have revealed the interaction between non-apoptotic RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, and necroptosis exhibit synergistic antitumor immune responses while possibly exerting inhibitory effects on antitumor immune responses. Thus, targeted therapies (inducers or inhibitors) against autophagy, ferroptosis, pyroptosis, and necroptosis in combination with immunotherapy may exert potent antitumor activity, even in tumors resistant to ICIs. This review summarizes the multilevel relationship between antitumor immunity and non-apoptotic RCD, including autophagy, ferroptosis, pyroptosis, and necroptosis, and the potential targeting application of non-apoptotic RCD to improve the efficacy of immunotherapy in malignancy.

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“…Since the phenotype of SpiB cKO mice in the TD immune response was apparent only in the late B mem cells and their recall response, we suspected the function of SpiB to be more related to the maintenance of B mem cells rather than their generation. Previous studies have shown that autophagy is one of the mechanisms to inhibit apoptosis and to support the survival of memory T and B cells ( 36 – 39 ). Therefore, we analyzed the expression levels of anti-apoptotic genes and autophagy genes in GC B and B mem cells sorted from SpiB cKO and SpiB WT mice 14 days after immunization with NP-CGG.…”

Section: Resultsmentioning

confidence: 99%

SpiB regulates the expression of B-cell-related genes and increases the longevity of memory B cells

Horiuchi,

Koike,

Takebuchi

et al. 2023

Front. Immunol.

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Generation of memory B cells is one of the key features of adaptive immunity as they respond rapidly to re-exposure to the antigen and generate functional antibodies. Although the functions of memory B cells are becoming clearer, the regulation of memory B cell generation and maintenance is still not well understood. Here we found that transcription factor SpiB is expressed in some germinal center (GC) B cells and memory B cells and participates in the maintenance of memory B cells. Overexpression and knockdown analyses revealed that SpiB suppresses plasma cell differentiation by suppressing the expression of Blimp1 while inducing Bach2 in the in-vitro-induced germinal center B (iGB) cell culture system, and that SpiB facilitates in-vivo appearance of memory-like B cells derived from the iGB cells. Further analysis in IgG1+ cell-specific SpiB conditional knockout (cKO) mice showed that function of SpiB is critical for the generation of late memory B cells but not early memory B cells or GC B cells. Gene expression analysis suggested that SpiB-dependent suppression of plasma cell differentiation is independent of the expression of Bach2. We further revealed that SpiB upregulates anti-apoptosis and autophagy genes to control the survival of memory B cells. These findings indicate the function of SpiB in the generation of long-lasting memory B cells to maintain humoral memory.

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Protection of Quiescence and Longevity of IgG Memory B Cells by Mitochondrial Autophagy

Cited by 9 publications

References 93 publications

Expansion of Antigen- Specific Memory Cells as a Potential Booster for Food Tolerance Induction

Expansion of Antigen- Specific Memory Cells as a Potential Booster for Food Tolerance Induction

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

SpiB regulates the expression of B-cell-related genes and increases the longevity of memory B cells

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